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For: Frixen UH, Behrens J, Sachs M, Eberle G, Voss B, Warda A, Löchner D, Birchmeier W. E-cadherin-mediated cell-cell adhesion prevents invasiveness of human carcinoma cells. J Cell Biol 1991;113:173-85. [PMID: 2007622 PMCID: PMC2288921 DOI: 10.1083/jcb.113.1.173] [Citation(s) in RCA: 1162] [Impact Index Per Article: 34.2] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/29/2022] Open

For:	Frixen UH, Behrens J, Sachs M, Eberle G, Voss B, Warda A, Löchner D, Birchmeier W. E-cadherin-mediated cell-cell adhesion prevents invasiveness of human carcinoma cells. J Cell Biol 1991;113:173-85. [PMID: 2007622 PMCID: PMC2288921 DOI: 10.1083/jcb.113.1.173] [Citation(s) in RCA: 1162] [Impact Index Per Article: 34.2] [Reference Citation Analysis] [What about the content of this article? (0)] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/29/2022] Open

Number

Cited by Other Article(s)

Castaneda M, den Hollander P, Werden S, Ramirez-Peña E, Vasaikar SV, Kuburich NA, Gould C, Soundararajan R, Mani SA. β-Catenin Drives the FOXC2-Mediated Epithelial-Mesenchymal Transition and Acquisition of Stem Cell Properties. Cancers (Basel) 2025;17:1114. [PMID: 40227590 PMCID: PMC11987759 DOI: 10.3390/cancers17071114] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/01/2024] [Revised: 03/03/2025] [Accepted: 03/17/2025] [Indexed: 04/15/2025] Open

Affiliation(s)

Maria Castaneda Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Research Center, Houston, TX 77030, USA; (M.C.); (R.S.)
Petra den Hollander Department of Pathology and Laboratory Medicine, The Warren Alpert Medical School, Brown University, Providence, RI 02912, USA; (P.d.H.); (N.A.K.); (C.G.) Legorreta Cancer Center, The Warren Alpert Medical School, Brown University, Providence, RI 02912, USA
Steve Werden Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Research Center, Houston, TX 77030, USA; (M.C.); (R.S.)
Esmeralda Ramirez-Peña Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Research Center, Houston, TX 77030, USA; (M.C.); (R.S.)
Suhas V. Vasaikar Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Research Center, Houston, TX 77030, USA; (M.C.); (R.S.)
Nick A. Kuburich Department of Pathology and Laboratory Medicine, The Warren Alpert Medical School, Brown University, Providence, RI 02912, USA; (P.d.H.); (N.A.K.); (C.G.) Legorreta Cancer Center, The Warren Alpert Medical School, Brown University, Providence, RI 02912, USA
Claire Gould Department of Pathology and Laboratory Medicine, The Warren Alpert Medical School, Brown University, Providence, RI 02912, USA; (P.d.H.); (N.A.K.); (C.G.) Legorreta Cancer Center, The Warren Alpert Medical School, Brown University, Providence, RI 02912, USA
Rama Soundararajan Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Research Center, Houston, TX 77030, USA; (M.C.); (R.S.)
Sendurai A. Mani Department of Pathology and Laboratory Medicine, The Warren Alpert Medical School, Brown University, Providence, RI 02912, USA; (P.d.H.); (N.A.K.); (C.G.) Legorreta Cancer Center, The Warren Alpert Medical School, Brown University, Providence, RI 02912, USA

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Zhang Z, Wang J, Wuethrich A, Trau M. Conventional techniques and emerging nanotechnologies for early detection of cancer metastasis via epithelial-mesenchymal transition monitoring. Natl Sci Rev 2025;12:nwae452. [PMID: 39926198 PMCID: PMC11804803 DOI: 10.1093/nsr/nwae452] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/23/2024] [Revised: 10/31/2024] [Accepted: 11/10/2024] [Indexed: 02/11/2025] Open

Guan Y, Chen Y, Lin R, Mo T, Li S, Cao Y, Yin T, Diao L, Li Y. Endometriosis: A new perspective on epigenetics and oxidative stress. J Reprod Immunol 2025;169:104462. [PMID: 40010026 DOI: 10.1016/j.jri.2025.104462] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/08/2024] [Revised: 01/07/2025] [Accepted: 02/20/2025] [Indexed: 02/28/2025]

Affiliation(s)

Yu Guan Reproductive Medicine Center, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China
Yawen Chen Shenzhen Key Laboratory of Reproductive Immunology for Peri-implantation, Shenzhen Zhongshan Institute for Reproductive Medicine and Genetics, Shenzhen Zhongshan Obstetrics & Gynecology Hospital (formerly Shenzhen Zhongshan Urology Hospital), China; Guangdong Engineering Technology Research Center of Reproductive Immunology for Peri-implantation, China
Rong Lin Shenzhen Key Laboratory of Reproductive Immunology for Peri-implantation, Shenzhen Zhongshan Institute for Reproductive Medicine and Genetics, Shenzhen Zhongshan Obstetrics & Gynecology Hospital (formerly Shenzhen Zhongshan Urology Hospital), China; Guangdong Engineering Technology Research Center of Reproductive Immunology for Peri-implantation, China
Tinghui Mo Reproductive Medicine Center, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China
Shiyu Li Reproductive Medicine Center, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China
Ying Cao Reproductive Medicine Center, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China
Tailang Yin Reproductive Medicine Center, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
Lianghui Diao Shenzhen Key Laboratory of Reproductive Immunology for Peri-implantation, Shenzhen Zhongshan Institute for Reproductive Medicine and Genetics, Shenzhen Zhongshan Obstetrics & Gynecology Hospital (formerly Shenzhen Zhongshan Urology Hospital), China; Guangdong Engineering Technology Research Center of Reproductive Immunology for Peri-implantation, China.
Yuye Li Shenzhen Key Laboratory of Reproductive Immunology for Peri-implantation, Shenzhen Zhongshan Institute for Reproductive Medicine and Genetics, Shenzhen Zhongshan Obstetrics & Gynecology Hospital (formerly Shenzhen Zhongshan Urology Hospital), China; Guangdong Engineering Technology Research Center of Reproductive Immunology for Peri-implantation, China.

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Udroiu I, Todaro F, Vitaliti A, Palmieri D, Guida E, Perilli G, Duranti L, D'Ottavi C, Mattei M, Dolci S, Paradossi G, Bedini A, Silvestri I, Sgura A, Domenici F. Low-intensity pulsed ultrasound induces multifaced alterations in chromosome segregation, cytoskeletal filaments and cell junctions. Sci Rep 2025;15:4964. [PMID: 39929986 PMCID: PMC11811000 DOI: 10.1038/s41598-025-88569-1] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/28/2024] [Accepted: 01/29/2025] [Indexed: 02/13/2025] Open

Affiliation(s)

Ion Udroiu Department of Sciences, Università Roma Tre, Viale G. Marconi 446, Rome, 00146, Italy
Federica Todaro Section of Endocrinology and Metabolic Diseases, Department of Systems Medicine, University of Rome "Tor Vergata", Rome, 00133, Italy Department of Chemical Science and Technologies, University of Rome "Tor Vergata", Rome, 00133, Italy
Alessandra Vitaliti Department of Chemical Science and Technologies, University of Rome "Tor Vergata", Rome, 00133, Italy
Damiano Palmieri Medical Physics Unit, Bambino Gesù Children's Hospital, IRCCS, Rome, 00165, Italy
Eugenia Guida Department of Biomedicine and Prevention, University Hospital of Rome "Tor Vergata", Rome, 00133, Italy
Giulia Perilli Department of Chemical Science and Technologies, University of Rome "Tor Vergata", Rome, 00133, Italy
Leonardo Duranti Department of Chemical Science and Technologies, University of Rome "Tor Vergata", Rome, 00133, Italy
Cadia D'Ottavi Department of Chemical Science and Technologies, University of Rome "Tor Vergata", Rome, 00133, Italy
Maurizio Mattei Interdepartmental Center for Comparative Medicine, Alternative Techniques and Aquaculture (CIMETA), University of Rome "Tor Vergata", Via Montpellier 1, Rome, 00133, Italy Department of Biology, University of Rome "Tor Vergata", Rome, 00133, Italy
Susanna Dolci Department of Biomedicine and Prevention, University Hospital of Rome "Tor Vergata", Rome, 00133, Italy
Gaio Paradossi Department of Chemical Science and Technologies, University of Rome "Tor Vergata", Rome, 00133, Italy
Angelico Bedini Department of Technological Innovations and Safety of Plants, Products and Anthropic Settlements (DIT), Italian National Institute for Insurance against Accidents at Work, Inail, Rome, 00144, Italy
Ida Silvestri Department of Molecular Medicine, Sapienza University, Viale Regina Elena 324, Rome, 00161, Italy
Antonella Sgura Department of Sciences, Università Roma Tre, Viale G. Marconi 446, Rome, 00146, Italy
Fabio Domenici Department of Chemical Science and Technologies, University of Rome "Tor Vergata", Rome, 00133, Italy.

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Schaller L, Gudermann T, Dietrich A. TRPV4 Mediates Alveolar Epithelial Barrier Integrity and Induces ADAM10-Driven E-Cadherin Shedding. Cells 2024;13:1717. [PMID: 39451235 PMCID: PMC11506556 DOI: 10.3390/cells13201717] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/23/2024] [Revised: 10/11/2024] [Accepted: 10/15/2024] [Indexed: 10/26/2024] Open

Kolokotronis T, Majchrzak-Stiller B, Buchholz M, Mense V, Strotmann J, Peters I, Skrzypczyk L, Liffers ST, Menkene LM, Wagner M, Glanemann M, Betsou F, Ammerlaan W, Schmidt R, Schröder C, Uhl W, Braumann C, Höhn P. Differential miRNA and Protein Expression Reveals miR-1285, Its Targets TGM2 and CDH-1, as Well as CD166 and S100A13 as Potential New Biomarkers in Patients with Diabetes Mellitus and Pancreatic Adenocarcinoma. Cancers (Basel) 2024;16:2726. [PMID: 39123454 PMCID: PMC11311671 DOI: 10.3390/cancers16152726] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/21/2024] [Revised: 07/16/2024] [Accepted: 07/30/2024] [Indexed: 08/12/2024] Open

Affiliation(s)

Theodoros Kolokotronis St. Josef Hospital Bochum, Surgical Clinic, Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany; (B.M.-S.); (M.B.); (V.M.); (J.S.); (I.P.); (L.S.); (W.U.); (C.B.); (P.H.) Institute of Pathology and Surgical Clinic, University Hospital of Saarland, Kirrberger Str. 100, 66424 Homburg, Germany; (L.M.M.); (M.W.)
Britta Majchrzak-Stiller St. Josef Hospital Bochum, Surgical Clinic, Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany; (B.M.-S.); (M.B.); (V.M.); (J.S.); (I.P.); (L.S.); (W.U.); (C.B.); (P.H.)
Marie Buchholz St. Josef Hospital Bochum, Surgical Clinic, Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany; (B.M.-S.); (M.B.); (V.M.); (J.S.); (I.P.); (L.S.); (W.U.); (C.B.); (P.H.)
Vanessa Mense St. Josef Hospital Bochum, Surgical Clinic, Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany; (B.M.-S.); (M.B.); (V.M.); (J.S.); (I.P.); (L.S.); (W.U.); (C.B.); (P.H.)
Johanna Strotmann St. Josef Hospital Bochum, Surgical Clinic, Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany; (B.M.-S.); (M.B.); (V.M.); (J.S.); (I.P.); (L.S.); (W.U.); (C.B.); (P.H.)
Ilka Peters St. Josef Hospital Bochum, Surgical Clinic, Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany; (B.M.-S.); (M.B.); (V.M.); (J.S.); (I.P.); (L.S.); (W.U.); (C.B.); (P.H.)
Lea Skrzypczyk St. Josef Hospital Bochum, Surgical Clinic, Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany; (B.M.-S.); (M.B.); (V.M.); (J.S.); (I.P.); (L.S.); (W.U.); (C.B.); (P.H.)
Sven-Thorsten Liffers University Hospital Essen, Bridging Institute for Experimental Tumor Therapy, West German Tumor Center Essen, Hufelandstr. 55, 45147 Essen, Germany;
Louise Massia Menkene Institute of Pathology and Surgical Clinic, University Hospital of Saarland, Kirrberger Str. 100, 66424 Homburg, Germany; (L.M.M.); (M.W.)
Mathias Wagner Institute of Pathology and Surgical Clinic, University Hospital of Saarland, Kirrberger Str. 100, 66424 Homburg, Germany; (L.M.M.); (M.W.)
Matthias Glanemann Institute of Pathology and Surgical Clinic, University Hospital of Saarland, Kirrberger Str. 100, 66424 Homburg, Germany; (L.M.M.); (M.W.)
Fay Betsou CRBIP, Institut Pasteur, Université Paris Cite, 25 rue du Dr Roux, 75015 Paris, France;
Wim Ammerlaan IBBL (Integrated BioBank of Luxembourg), 1, Rue Louis Rech, L-3555 Dudelange, Luxembourg;
Ronny Schmidt Sciomics GmbH, Karl-Landsteiner Str. 6, 69151 Heidelberg, Germany; (R.S.); (C.S.)
Christoph Schröder Sciomics GmbH, Karl-Landsteiner Str. 6, 69151 Heidelberg, Germany; (R.S.); (C.S.)
Waldemar Uhl St. Josef Hospital Bochum, Surgical Clinic, Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany; (B.M.-S.); (M.B.); (V.M.); (J.S.); (I.P.); (L.S.); (W.U.); (C.B.); (P.H.)
Chris Braumann St. Josef Hospital Bochum, Surgical Clinic, Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany; (B.M.-S.); (M.B.); (V.M.); (J.S.); (I.P.); (L.S.); (W.U.); (C.B.); (P.H.) Department of General, Visceral and Vascular Surgery, EvK Gelsenkirchen, University Duisburg-Essen, Munckelstr. 27, 45879 Gelsenkirchen, Germany
Philipp Höhn St. Josef Hospital Bochum, Surgical Clinic, Ruhr-University Bochum, Gudrunstr. 56, 44791 Bochum, Germany; (B.M.-S.); (M.B.); (V.M.); (J.S.); (I.P.); (L.S.); (W.U.); (C.B.); (P.H.)

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Borini Etichetti C, Arel Zalazar E, Di Benedetto C, Cocordano N, Valente S, Bicciato S, Menacho-Márquez M, Larocca MC, Girardini J. Isoprenylcysteine carboxyl methyltransferase (ICMT) promotes invadopodia formation and metastasis in cancer cells. Biochimie 2024;222:28-36. [PMID: 38301884 DOI: 10.1016/j.biochi.2024.01.015] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/11/2023] [Revised: 01/16/2024] [Accepted: 01/29/2024] [Indexed: 02/03/2024]

Noronha C, Ribeiro AS, Carvalho R, Mendes N, Reis J, Faria CC, Taipa R, Paredes J. Cadherin Expression Profiles Define Glioblastoma Differentiation and Patient Prognosis. Cancers (Basel) 2024;16:2298. [PMID: 39001361 PMCID: PMC11240393 DOI: 10.3390/cancers16132298] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/31/2024] [Revised: 06/14/2024] [Accepted: 06/18/2024] [Indexed: 07/16/2024] Open

Affiliation(s)

Carolina Noronha Neurosurgery Department, Hospital de Santo António, Centro Hospitalar e Universitário do Porto, 4050-366 Porto, Portugal Cancer Metastasis, i3S, Institute for Research and Innovation in Health, University of Porto, 4200-135 Porto, Portugal FMUP-Faculty of Medicine, University of Porto, 4200-135 Porto, Portugal
Ana Sofia Ribeiro Cancer Metastasis, i3S, Institute for Research and Innovation in Health, University of Porto, 4200-135 Porto, Portugal IPATIMUP-Institute of Molecular Pathology and Immunology, University of Porto, 4200-135 Porto, Portugal
Rita Carvalho Cancer Metastasis, i3S, Institute for Research and Innovation in Health, University of Porto, 4200-135 Porto, Portugal IPATIMUP-Institute of Molecular Pathology and Immunology, University of Porto, 4200-135 Porto, Portugal
Nuno Mendes IPATIMUP-Institute of Molecular Pathology and Immunology, University of Porto, 4200-135 Porto, Portugal Histology and Electron Microscopy, i3S, Institute for Research and Innovation in Health, University of Porto, 4200-135 Porto, Portugal
Joaquim Reis Neurosurgery Department, Hospital de Santo António, Centro Hospitalar e Universitário do Porto, 4050-366 Porto, Portugal
Claudia C Faria Neurosurgery Department, Hospital de Santa Maria, Centro Hospitalar Universitário Lisboa Norte, 1649-028 Lisbon, Portugal IMM-Instituto de Medicina Molecular João Lobo Antunes, Faculty of Medicine, University of Lisbon, 1649-028 Lisbon, Portugal
Ricardo Taipa Neuropathology Department, Hospital de Santo António, Centro Hospitalar Universitário de Santo António, 4050-342 Porto, Portugal UMIB-Unit for Multidisciplinary Research in Biomedicine, ICBAS-School of Medicine and Biomedical Sciences, University of Porto, 4050-346 Porto, Portugal ITR-Laboratory for Integrative and Translational Research in Population Health, 4050-600 Porto, Portugal
Joana Paredes Cancer Metastasis, i3S, Institute for Research and Innovation in Health, University of Porto, 4200-135 Porto, Portugal FMUP-Faculty of Medicine, University of Porto, 4200-135 Porto, Portugal IPATIMUP-Institute of Molecular Pathology and Immunology, University of Porto, 4200-135 Porto, Portugal

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Souza A, Kevin M, Rodriguez BJ, Reynaud EG. The use of fluid-phase 3D printing to pattern alginate-gelatin hydrogel properties to guide cell growth and behaviourin vitro. Biomed Mater 2024;19:045024. [PMID: 38810635 DOI: 10.1088/1748-605x/ad51bf] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/01/2023] [Accepted: 05/29/2024] [Indexed: 05/31/2024]

Abstract

Three-dimensional (3D) (bio)printing technology has boosted the advancement of the biomedical field. However, tissue engineering is an evolving field and (bio)printing biomimetic constructions for tissue formation is still a challenge. As a new methodology to facilitate the construction of more complex structures, we suggest the use of the fluid-phase 3D printing to pattern the scaffold's properties. The methodology consists of an exchangeable fluid-phase printing medium in which the constructions are fabricated and patterned during the printing process. Using the fluid-phase methodology, the biological and mechanical properties can be tailored promoting cell behaviour guidance and compartmentalization. In this study, we first assessed different formulations of alginate/gelatin to create a stable substrate capable to promote massive cell colonizationin vitroover time. Overall, formulations with lower gelatin content and 2-(N-morpholino)ethanesulfonic acid (MES) buffer as a solvent showed better stability under cell culture conditions and enhanced U2OS cell growth. Next, the fluid-phase showed better printing fidelity and resolution in comparison to air printing as it diminished the collapsing and the spread of the hydrogel strand. In sequence, the fluid-phase methodology was used to create functionalized alginate-gelatin-arginylglycylaspartic acid peptide (RGD) hydrogels via carbodiimides chemistry. The alginate-gelatin-RGD hydrogels showed an increase of 2.97-fold in cell growth and more spread substrate colonization in comparison to alginate-gelatin hydrogel. Moreover, the fluid-phase methodology was used to add RGD molecules to pre-determined parts of the alginate-gelatin substrate during the printing process promoting U2OS cell compartmentalization. In addition, different substrate stiffnesses were also created via fluid-phase by crosslinking the hydrogel with different concentrations of CaCl2during the printing process. As a result, the U2OS cells were also compartmentalized on the stiffer parts of the printings. Finally, our results showed that by combining stiffer hydrogel with RGD increasing concentrations we can create a synergetic effect and boost cell metabolism by up to 3.17-fold. This work presents an idea of a new printing process for tailoring multiple parameters in hydrogel substrates by using fluid-phase to generate more faithful replication of thein vivoenvironment.

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Filho FDSA, Santiago LH, Fernandes ACN, Korn GP, Pontes PADL, Camponês do Brasil ODO. Preliminary Correlation of the Immunoexpression of Cathepsin B and E-Cadherin Proteins in Vocal Fold Leukoplakia. J Voice 2024;38:760-767. [PMID: 34663533 DOI: 10.1016/j.jvoice.2021.08.005] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/21/2021] [Revised: 08/09/2021] [Accepted: 08/11/2021] [Indexed: 11/17/2022]

Wang Y, Xiong Y, Shi K, Effah CY, Song L, He L, Liu J. DNA nanostructures for exploring cell-cell communication. Chem Soc Rev 2024;53:4020-4044. [PMID: 38444346 DOI: 10.1039/d3cs00944k] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 03/07/2024]

Jackson CE, Green NH, English WR, Claeyssens F. The use of microphysiological systems to model metastatic cancer. Biofabrication 2024;16:032002. [PMID: 38579739 DOI: 10.1088/1758-5090/ad3b70] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/13/2023] [Accepted: 04/05/2024] [Indexed: 04/07/2024]

Xiao Y, Zhou L, Andl T, Zhang Y. YAP1 controls the N-cadherin-mediated tumor-stroma interaction in melanoma progression. Oncogene 2024;43:884-898. [PMID: 38308096 PMCID: PMC10942861 DOI: 10.1038/s41388-024-02953-1] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/25/2023] [Revised: 01/17/2024] [Accepted: 01/18/2024] [Indexed: 02/04/2024]

Tessier CE, Dupuy AMM, Pelé T, Juin PP, Lees JA, Guen VJ. EMT and primary ciliogenesis: For better or worse in sickness and in health. Genesis 2024;62:e23568. [PMID: 37946671 DOI: 10.1002/dvg.23568] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/09/2023] [Revised: 08/23/2023] [Accepted: 10/13/2023] [Indexed: 11/12/2023]

Belut DR, Lima EDO, Zanini MA, Galvani AF, Furtado FB, Ferrasi AC. CDH1 hypermethylation: a potential molecular pathway for invasiveness in glioblastoma. Eur J Cancer Prev 2024;33:73-75. [PMID: 37401481 DOI: 10.1097/cej.0000000000000824] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 07/05/2023]

Golconda P, Andrade-Medina M, Oberstein A. Subconfluent ARPE-19 Cells Display Mesenchymal Cell-State Characteristics and Behave like Fibroblasts, Rather Than Epithelial Cells, in Experimental HCMV Infection Studies. Viruses 2023;16:49. [PMID: 38257749 PMCID: PMC10821009 DOI: 10.3390/v16010049] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/02/2023] [Revised: 12/20/2023] [Accepted: 12/25/2023] [Indexed: 01/24/2024] Open

Abstract

Human cytomegalovirus (HCMV) has a broad cellular tropism and epithelial cells are important physiological targets during infection. The retinal pigment epithelial cell line ARPE-19 has been used to model HCMV infection in epithelial cells for decades and remains a commonly used cell type for studying viral entry, replication, and the cellular response to infection. We previously found that ARPE-19 cells, despite being derived from an epithelial cell explant, express extremely low levels of canonical epithelial proteins, such as E-cadherin and EpCAM. Here, we perform comparative studies of ARPE-19 and additional epithelial cell lines with strong epithelial characteristics. We find that ARPE-19 cells cultured under subconfluent conditions resemble mesenchymal fibroblasts, rather than epithelial cells; this is consistent with previous studies showing that ARPE-19 cultures require extended periods of high confluency culture to maintain epithelial characteristics. By reanalyzing public gene expression data and using machine learning, we find evidence that ARPE-19 cultures maintained across many labs exhibit mesenchymal characteristics and that the majority of studies employing ARPE-19 use them in a mesenchymal state. Lastly, by performing experimental HCMV infections across mesenchymal and epithelial cell lines, we find that ARPE-19 cells behave like mesenchymal fibroblasts, producing logarithmic yields of cell-free infectious progeny, while cell lines with strong epithelial character exhibit an atypical infectious cycle and naturally restrict the production of cell-free progeny. Our work highlights important characteristics of the ARPE-19 cell line and suggests that subconfluent ARPE-19 cells may not be optimal for modeling epithelial infection with HCMV or other human viruses. It also suggests that HCMV biosynthesis and/or spread may occur quite differently in epithelial cells compared to mesenchymal cells. These differences could contribute to viral persistence or pathogenesis in epithelial tissues.

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Alatawi FS, Faridi U. Anticancer and anti-metastasis activity of 1,25 dihydroxycholecalciferols and genistein in MCF-7 and MDA-MB-231 breast cancer cell lines. Heliyon 2023;9:e21975. [PMID: 38034665 PMCID: PMC10682641 DOI: 10.1016/j.heliyon.2023.e21975] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/28/2022] [Revised: 11/01/2023] [Accepted: 11/01/2023] [Indexed: 12/02/2023] Open

Xia YT, Zhang YQ, Chen L, Min L, Huang D, Zhang Y, Li C, Li ZH. Suppression of migration and invasion by taraxerol in the triple-negative breast cancer cell line MDA-MB-231 via the ERK/Slug axis. PLoS One 2023;18:e0291693. [PMID: 37751436 PMCID: PMC10522031 DOI: 10.1371/journal.pone.0291693] [Citation(s) in RCA: 2] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/05/2023] [Accepted: 08/26/2023] [Indexed: 09/28/2023] Open

Xio Y, Zhou L, Andl T, Zhang Y. YAP1 controls the N-cadherin-mediated tumor-stroma interaction in melanoma progression. RESEARCH SQUARE 2023:rs.3.rs-2944243. [PMID: 37546745 PMCID: PMC10402251 DOI: 10.21203/rs.3.rs-2944243/v3] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 08/08/2023]

Tierno D, Azzalini E, Farra R, Drioli S, Felluga F, Lazzarino M, Grassi G, Dapas B, Bonin S. Nanomechanical Characterization of Ovarian Cancer Cell Lines as a Marker of Response to 2c Treatment. Int J Mol Sci 2023;24:7230. [PMID: 37108391 PMCID: PMC10139025 DOI: 10.3390/ijms24087230] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/16/2023] [Revised: 04/07/2023] [Accepted: 04/11/2023] [Indexed: 04/29/2023] Open

Huang W, Fu C, Yan J. Single-Cell Quantification of the Mechanical Stability of Cell-Cell Adherens Junction Using Glass Micropipettes. Methods Mol Biol 2023;2600:267-280. [PMID: 36587103 DOI: 10.1007/978-1-0716-2851-5_17] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 06/17/2023]

Luís C, Soares R, Fernandes R, Botelho M. Cell-adhesion Molecules as Key Mechanisms of Tumor Invasion: The Case of Breast Cancer. Curr Mol Med 2023;23:147-160. [PMID: 34365950 DOI: 10.2174/1566524021666210806155231] [Citation(s) in RCA: 5] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/03/2020] [Revised: 03/10/2021] [Accepted: 03/23/2021] [Indexed: 12/16/2022]

Quereda C, Pastor À, Martín-Nieto J. Involvement of abnormal dystroglycan expression and matriglycan levels in cancer pathogenesis. Cancer Cell Int 2022;22:395. [PMID: 36494657 PMCID: PMC9733019 DOI: 10.1186/s12935-022-02812-7] [Citation(s) in RCA: 11] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/24/2022] [Accepted: 11/28/2022] [Indexed: 12/13/2022] Open

Abstract

Dystroglycan (DG) is a glycoprotein composed of two subunits that remain non-covalently bound at the plasma membrane: α-DG, which is extracellular and heavily O-mannosyl glycosylated, and β-DG, an integral transmembrane polypeptide. α-DG is involved in the maintenance of tissue integrity and function in the adult, providing an O-glycosylation-dependent link for cells to their extracellular matrix. β-DG in turn contacts the cytoskeleton via dystrophin and participates in a variety of pathways transmitting extracellular signals to the nucleus. Increasing evidence exists of a pivotal role of DG in the modulation of normal cellular proliferation. In this context, deficiencies in DG glycosylation levels, in particular those affecting the so-called matriglycan structure, have been found in an ample variety of human tumors and cancer-derived cell lines. This occurs together with an underexpression of the DAG1 mRNA and/or its α-DG (core) polypeptide product or, more frequently, with a downregulation of β-DG protein levels. These changes are in general accompanied in tumor cells by a low expression of genes involved in the last steps of the α-DG O-mannosyl glycosylation pathway, namely POMT1/2, POMGNT2, CRPPA, B4GAT1 and LARGE1/2. On the other hand, a series of other genes acting earlier in this pathway are overexpressed in tumor cells, namely DOLK, DPM1/2/3, POMGNT1, B3GALNT2, POMK and FKTN, hence exerting instead a pro-oncogenic role. Finally, downregulation of β-DG, altered β-DG processing and/or impaired β-DG nuclear levels are increasingly found in human tumors and cell lines. It follows that DG itself, particular genes/proteins involved in its glycosylation and/or their interactors in the cell could be useful as biomarkers of certain types of human cancer, and/or as molecular targets of new therapies addressing these neoplasms.

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Hidari K, Nakamoto Y, Sakurai K, Sakurai Y, Nibe K, Nakamoto M. Case report: Presumptive subcutaneous malignant peripheral nerve sheath tumor with intracranial invasion and osteolysis in the posterior fossa of a dog. Front Vet Sci 2022;9:977099. [PMID: 36425125 PMCID: PMC9679371 DOI: 10.3389/fvets.2022.977099] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/24/2022] [Accepted: 10/12/2022] [Indexed: 11/11/2022] Open

Malmi-Kakkada AN, Sinha S, Li X, Thirumalai D. Adhesion strength between cells regulate nonmonotonic growth by a biomechanical feedback mechanism. Biophys J 2022;121:3719-3729. [PMID: 35505608 PMCID: PMC9617137 DOI: 10.1016/j.bpj.2022.04.032] [Citation(s) in RCA: 11] [Impact Index Per Article: 3.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/17/2021] [Revised: 03/22/2022] [Accepted: 04/26/2022] [Indexed: 11/24/2022] Open

Park KB, Kim EY, Chin H, Yoon DJ, Jun KH. Leptin stimulates migration and invasion and maintains cancer stem‑like properties in gastric cancer cells. Oncol Rep 2022;48:162. [PMID: 35866593 PMCID: PMC9350977 DOI: 10.3892/or.2022.8377] [Citation(s) in RCA: 9] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/16/2022] [Accepted: 07/07/2022] [Indexed: 11/29/2022] Open

Abstract

Obesity is a risk factor for various types of cancer. Leptin, an adipocyte-derived hormone, may stimulate the proliferation of gastric cancer cells. However, the effect of leptin and underlying mechanism in gastric cancer remain unclear. In the present study, the role of leptin in gastric cancer was evaluated. The effect of leptin on the JAK-STAT and MEK signaling pathways was investigated in gastric cancer cells using wound-healing and cell invasion assays, immunoblotting and inhibition studies. Cancer-initiating cells derived from gastric cancer cells were used to investigate the effect of leptin on the maintenance of stemness and epithelial-mesenchymal transition (EMT) by immunoblotting. Clinicopathological characteristics including the serum leptin level and overall survival (OS) were analyzed in patients with (n=23) and without (n=23) obesity. Leptin induced the migration and invasion of gastric cancer cells by activating AKT and ERK and upregulating vascular endothelial growth factor (VEGF). Leptin increased the mRNA and protein levels of markers of stemness (CD44) and the EMT (Snail and N-cadherin). Pharmacological inhibitors of the JAK-STAT and MEK signaling pathways decreased leptin-induced migration and invasion, and the expression of VEGF. Obesity was associated with an elevated leptin level and body mass index was positively correlated with the leptin level (P=0.001 for both). The 5-year OS rate was not significantly different between the two groups (P=0.098). Leptin stimulates the migration and invasion of gastric cancer cells by activating the JAK-STAT and MEK pathways, and contributes to the maintenance of cancer stemness and metastatic potential. The present findings support an adverse effect of obesity in gastric cancer. Consequently, targeting of leptin-associated signaling pathways may have therapeutic potential for gastric cancer.

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Levenson AS. Dietary stilbenes as modulators of specific miRNAs in prostate cancer. Front Pharmacol 2022;13:970280. [PMID: 36091792 PMCID: PMC9449421 DOI: 10.3389/fphar.2022.970280] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/15/2022] [Accepted: 07/20/2022] [Indexed: 11/13/2022] Open

Mari V, Angerilli V, Munari G, Scarpa M, Bao QR, Pucciarelli S, Fassan M, Spolverato G. Molecular Determinants of Peritoneal Dissemination in Gastric Adenocarcinoma. Dig Dis 2022;41:49-65. [PMID: 35940137 DOI: 10.1159/000526333] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/12/2022] [Accepted: 07/25/2022] [Indexed: 02/02/2023]

Guo X, Li Y, Wan B, Lv Y, Wang X, Liu G, Wang P. KAT7 promoted gastric cancer progression through promoting YAP1 activation. Pathol Res Pract 2022;237:154020. [PMID: 35868058 DOI: 10.1016/j.prp.2022.154020] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/24/2022] [Revised: 07/05/2022] [Accepted: 07/12/2022] [Indexed: 11/29/2022]

Han P, Cao P, Yue J, Kong K, Hu S, Deng Y, Li L, Li F, Zhao B. Knockdown of hnRNPA1 Promotes NSCLC Metastasis and EMT by Regulating Alternative Splicing of LAS1L exon 9. Front Oncol 2022;12:837248. [PMID: 35814393 PMCID: PMC9260696 DOI: 10.3389/fonc.2022.837248] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/04/2022] [Accepted: 05/09/2022] [Indexed: 12/02/2022] Open

Corgnac S, Damei I, Gros G, Caidi A, Terry S, Chouaib S, Deloger M, Mami-Chouaib F. Cancer stem-like cells evade CD8⁺CD103⁺ tumor-resident memory T (T_RM) lymphocytes by initiating an epithelial-to-mesenchymal transition program in a human lung tumor model. J Immunother Cancer 2022;10:jitc-2022-004527. [PMID: 35418483 PMCID: PMC9014106 DOI: 10.1136/jitc-2022-004527] [Citation(s) in RCA: 18] [Impact Index Per Article: 6.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 03/23/2022] [Indexed: 02/06/2023] Open

Abstract

Background

Cancer stem cells (CSC) define a population of rare malignant cells endowed with ‘stemness’ properties, such as self-renewing, multipotency and tumorigenicity. They are responsible for tumor initiation and progression, and could be associated with resistance to immunotherapies by negatively regulating antitumor immune response and acquiring molecular features enabling escape from CD8 T-cell immunity. However, the immunological hallmarks of human lung CSC and their potential interactions with resident memory T (T_RM) cells within the tumor microenvironment have not been investigated.

Methods

We generated a non-small cell lung cancer model, including CSC line and clones, and autologous CD8⁺CD103⁺ T_RM and CD8⁺CD103⁻ non-T_RM clones, to dissect out immune properties of CSC and their susceptibility to specific T-cell-mediated cytotoxic activity.

Results

Unlike their parental tumor cells, lung CSC are characterized by the initiation of an epithelial-to-mesenchymal transition program defined by upregulation of the SNAIL1 transcription factor and downregulation of phosphorylated-GSK-3β and cell surface E-cadherin. Acquisition of a CSC profile results in partial resistance to T_RM-cell-mediated cytotoxicity, which correlates with decreased surface expression of the CD103 ligand E-cadherin and human leukocyte antigen-A2-neoepitope complexes. On the other hand, CSC gained expression of intercellular adhesion molecule (ICAM)-1 and thereby sensitivity to leukocyte function-associated antigen (LFA)-1-dependent non-T_RM-cell-mediated killing. Cytotoxicity is inhibited by anti-ICAM-1 and anti-major histocompatibility complex class I neutralizing antibodies further emphasizing the role of LFA-1/ICAM-1 interaction in T-cell receptor-dependent lytic function.

Conclusion

Our data support the rational design of immunotherapeutic strategies targeting CSC to optimize their responsiveness to local CD8⁺CD103⁺ T_RM cells for more efficient anticancer treatments.

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Flores AR, Rêma A, Mesquita JR, Taulescu M, Seixas F, Gärtner F, Amorim I. E-cadherin Expression in Canine Gastric Carcinomas: Association with Clinicopathological Parameters. Vet Sci 2022;9:172. [PMID: 35448670 PMCID: PMC9027758 DOI: 10.3390/vetsci9040172] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/11/2022] [Revised: 03/22/2022] [Accepted: 03/29/2022] [Indexed: 11/16/2022] Open

Affiliation(s)

Ana R. Flores ICBAS—School of Medicine and Biomedical Sciences, University of Porto, 4050-313 Porto, Portugal; (A.R.F.); (A.R.); (J.R.M.); (I.A.) Institute of Pathology and Molecular Immunology, University of Porto (IPATIMUP), 4200-465 Porto, Portugal; CECAV—Veterinary and Animal Research Center, University pf Trás-os-Montes and Alto Douro (UTAD), 5001-801 Vila Real, Portugal; Associate Laboratory for Animal and Veterinary Sciences (AL4AnimalS), 5001-801 Vila Real, Portugal
Alexandra Rêma ICBAS—School of Medicine and Biomedical Sciences, University of Porto, 4050-313 Porto, Portugal; (A.R.F.); (A.R.); (J.R.M.); (I.A.)
João R. Mesquita ICBAS—School of Medicine and Biomedical Sciences, University of Porto, 4050-313 Porto, Portugal; (A.R.F.); (A.R.); (J.R.M.); (I.A.) Epidemiology Research Unit (EPIUnit), Instituto de Saúde Pública, Universidade do Porto (ISPUP), 4050-600 Porto, Portugal
Marian Taulescu Department of Pathology, Faculty of Veterinary Medicine, University of Agricultural Sciences and Veterinary Medicine, 400372 Cluj-Napoca, Romania Synevovet Laboratory, 81 Pache Protopopescu, 021408 Bucharest, Romania
Fernanda Seixas CECAV—Veterinary and Animal Research Center, University pf Trás-os-Montes and Alto Douro (UTAD), 5001-801 Vila Real, Portugal; Associate Laboratory for Animal and Veterinary Sciences (AL4AnimalS), 5001-801 Vila Real, Portugal
Fátima Gärtner Institute of Pathology and Molecular Immunology, University of Porto (IPATIMUP), 4200-465 Porto, Portugal; i3S—Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal
Irina Amorim ICBAS—School of Medicine and Biomedical Sciences, University of Porto, 4050-313 Porto, Portugal; (A.R.F.); (A.R.); (J.R.M.); (I.A.) Institute of Pathology and Molecular Immunology, University of Porto (IPATIMUP), 4200-465 Porto, Portugal; i3S—Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal

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Morin C, Moyret-Lalle C, Mertani HC, Diaz JJ, Marcel V. Heterogeneity and dynamic of EMT through the plasticity of ribosome and mRNA translation. Biochim Biophys Acta Rev Cancer 2022;1877:188718. [PMID: 35304296 DOI: 10.1016/j.bbcan.2022.188718] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/05/2022] [Revised: 03/02/2022] [Accepted: 03/11/2022] [Indexed: 02/06/2023]

Habanjar O, Diab-Assaf M, Caldefie-Chezet F, Delort L. The Impact of Obesity, Adipose Tissue, and Tumor Microenvironment on Macrophage Polarization and Metastasis. BIOLOGY 2022;11:339. [PMID: 35205204 PMCID: PMC8869089 DOI: 10.3390/biology11020339] [Citation(s) in RCA: 23] [Impact Index Per Article: 7.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 11/29/2021] [Revised: 01/19/2022] [Accepted: 02/15/2022] [Indexed: 12/11/2022]

Abstract

Tumor metastasis is a major cause of death in cancer patients. It involves not only the intrinsic alterations within tumor cells, but also crosstalk between these cells and components of the tumor microenvironment (TME). Tumorigenesis is a complex and dynamic process, involving the following three main stages: initiation, progression, and metastasis. The transition between these stages depends on the changes within the extracellular matrix (ECM), in which tumor and stromal cells reside. This matrix, under the effect of growth factors, cytokines, and adipokines, can be morphologically altered, degraded, or reorganized. Many cancers evolve to form an immunosuppressive TME locally and create a pre-metastatic niche in other tissue sites. TME and pre-metastatic niches include myofibroblasts, immuno-inflammatory cells (macrophages), adipocytes, blood, and lymphatic vascular networks. Several studies have highlighted the adipocyte-macrophage interaction as a key driver of cancer progression and dissemination. The following two main classes of macrophages are distinguished: M1 (pro-inflammatory/anti-tumor) and M2 (anti-inflammatory/pro-tumor). These cells exhibit distinct microenvironment-dependent phenotypes that can promote or inhibit metastasis. On the other hand, obesity in cancer patients has been linked to a poor prognosis. In this regard, tumor-associated adipocytes modulate TME through the secretion of inflammatory mediators, which modulate and recruit tumor-associated macrophages (TAM). Hereby, this review describes the cellular and molecular mechanisms that link inflammation, obesity, and cancer. It provides a comprehensive overview of adipocytes and macrophages in the ECM as they control cancer initiation, progression, and invasion. In addition, it addresses the mechanisms of tumor anchoring and recruitment for M1, M2, and TAM macrophages, specifically highlighting their origin, classification, polarization, and regulatory networks, as well as their roles in the regulation of angiogenesis, invasion, metastasis, and immunosuppression, specifically highlighting the role of adipocytes in this process.

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Decoding Single Cell Morphology in Osteotropic Breast Cancer Cells for Dissecting Their Migratory, Molecular and Biophysical Heterogeneity. Cancers (Basel) 2022;14:cancers14030603. [PMID: 35158871 PMCID: PMC8833404 DOI: 10.3390/cancers14030603] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/26/2021] [Revised: 01/11/2022] [Accepted: 01/17/2022] [Indexed: 02/06/2023] Open

Nam MW, Kim CW, Choi KC. Epithelial-Mesenchymal Transition-Inducing Factors Involved in the Progression of Lung Cancers. Biomol Ther (Seoul) 2022;30:213-220. [PMID: 35039464 PMCID: PMC9047489 DOI: 10.4062/biomolther.2021.178] [Citation(s) in RCA: 17] [Impact Index Per Article: 5.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/26/2021] [Revised: 01/05/2022] [Accepted: 01/05/2022] [Indexed: 11/15/2022] Open

Jin Y, Park S, Park SY, Lee CY, Eum DY, Shim JW, Choi SH, Choi YJ, Park SJ, Heo K. G9a Knockdown Suppresses Cancer Aggressiveness by Facilitating Smad Protein Phosphorylation through Increasing BMP5 Expression in Luminal A Type Breast Cancer. Int J Mol Sci 2022;23:ijms23020589. [PMID: 35054776 PMCID: PMC8776044 DOI: 10.3390/ijms23020589] [Citation(s) in RCA: 13] [Impact Index Per Article: 4.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/01/2021] [Revised: 12/30/2021] [Accepted: 01/04/2022] [Indexed: 12/12/2022] Open

Puneeta N, Santosh T, Mishra I, Gaikwad P, Sahu A. Evaluation of e-cadherin and vimentin expression for different grades of oral epithelial dysplasia and oral squamous cell carcinoma - An immunohistochemical study. J Oral Maxillofac Pathol 2022;26:285-286. [PMID: 35968190 PMCID: PMC9364642 DOI: 10.4103/jomfp.jomfp_166_20] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/24/2020] [Revised: 07/10/2021] [Accepted: 10/19/2021] [Indexed: 11/04/2022] Open

Abstract

Background

Oral cancer is the 11^thcommon cancer in the world and ranks 6^thglobally in deaths. The incidence of oral cancer in India accounts for approximately 30%-40% of all cancers.

Aims and Objective

The present study was undertaken to evaluate the expression of Vimentin and E-cadherin in different grades of oral epithelial dysplasias (OEDs) and oral squamous cell carcinoma (OSCC).

Materials and Methods

Biopsies/blocks of oral cavity lesions were retrieved from the archives of the department. Normal oral mucosa (5 cases), oral epithelial dysplastic (60 cases) and different grades of OSCC (60 cases) evaluated by hematoxylin and eosin sections. Immunohistochemical analysis was done on the blocks and expression of E-cadherin and Vimentin was recorded.

Results

Our study included various grades of OED, OSCC and normal mucosa as control cases. The mean age of OED and OSCC was 49 and 56 years, respectively, with male predominance. Tobacco habit was present in approximately 90% cases, and buccal mucosa was the most commonly involved site in oral cavity with whitish patch and ulceroproliferative lesions being the common clinical presentations respectively. In OED, downregulation and altered localization of e-cadherin (81.6%) and increased expression of vimentin (52.3%) along with their concurrent increase in the stroma represent epithelial mesenchymal transition. In OSCC, reduction in expression (<50%) for e-cadherin (56.6%) with altered localization for e-cadherin was seen in 88.3% of OSCC along with neoexpression of vimentin in the epithelial cells was seen in 68.3% suggestive of mesenchymal phenotypic modification (P = 0.05).

Conclusion

It is very crucial to evaluate the invasiveness of dysplasia and tumor with specific molecular biomarker that may help in early prediction of malignancy and also guide in deciding best treatment strategy for established cases of malignancy.

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PCBP1 regulates the transcription and alternative splicing of metastasis‑related genes and pathways in hepatocellular carcinoma. Sci Rep 2021;11:23356. [PMID: 34857818 PMCID: PMC8640068 DOI: 10.1038/s41598-021-02642-z] [Citation(s) in RCA: 27] [Impact Index Per Article: 6.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/10/2021] [Accepted: 11/03/2021] [Indexed: 02/08/2023] Open

Shen L, Zhang S, Wang K, Wang X. Familial Breast Cancer: Disease Related Gene Mutations and Screening Strategies for Chinese Population. Front Oncol 2021;11:740227. [PMID: 34926254 PMCID: PMC8671637 DOI: 10.3389/fonc.2021.740227] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/12/2021] [Accepted: 11/12/2021] [Indexed: 12/24/2022] Open

Noronha C, Ribeiro AS, Taipa R, Castro DS, Reis J, Faria C, Paredes J. Cadherin Expression and EMT: A Focus on Gliomas. Biomedicines 2021;9:biomedicines9101328. [PMID: 34680444 PMCID: PMC8533397 DOI: 10.3390/biomedicines9101328] [Citation(s) in RCA: 45] [Impact Index Per Article: 11.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/19/2021] [Revised: 09/17/2021] [Accepted: 09/19/2021] [Indexed: 12/13/2022] Open

Lee HG, Lee KJ. Neighbor-enhanced diffusivity in dense, cohesive cell populations. PLoS Comput Biol 2021;17:e1009447. [PMID: 34555029 PMCID: PMC8491951 DOI: 10.1371/journal.pcbi.1009447] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/16/2021] [Revised: 10/05/2021] [Accepted: 09/13/2021] [Indexed: 12/30/2022] Open

Abstract

The dispersal or mixing of cells within cellular tissue is a crucial property for diverse biological processes, ranging from morphogenesis, immune action, to tumor metastasis. With the phenomenon of ‘contact inhibition of locomotion,’ it is puzzling how cells achieve such processes within a densely packed cohesive population. Here we demonstrate that a proper degree of cell-cell adhesiveness can, intriguingly, enhance the super-diffusive nature of individual cells. We systematically characterize the migration trajectories of crawling MDA-MB-231 cell lines, while they are in several different clustering modes, including freely crawling singles, cohesive doublets of two cells, quadruplets, and confluent population on two-dimensional substrate. Following data analysis and computer simulation of a simple cellular Potts model, which faithfully recapitulated all key experimental observations such as enhanced diffusivity as well as periodic rotation of cell-doublets and cell-quadruplets with mixing events, we found that proper combination of active self-propelling force and cell-cell adhesion is sufficient for generating the observed phenomena. Additionally, we found that tuning parameters for these two factors covers a variety of different collective dynamic states.

Dispersal or movement of cells within dense biological tissue is essential for diverse biological processes, ranging from pattern formation, immune action, to tumor metastasis. However, it is quite puzzling how cells acquire such ability when they are supposedly “caged” by neighboring cells. Here, we report an unusual property of (MDA-MB-231) breast cancer cells that diffuse more persistently within a densely packed population than when they are free to crawl around with little interference. This property is rather surprising since they prefer to stick together, forming clusters. Interestingly, however, we find that having sticky neighbors not only makes two active cells in contact periodically rotate, reminiscent of a ballroom dance, but also enhances the persistence of the cells within a dense population. These intriguing phenomena appear to be universal as they can be generated by a simple cellular Potts model with appropriate combination of active self-propulsion and cell-cell adhesion force.

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Karsten N, Kolben T, Mahner S, Beyer S, Meister S, Kuhn C, Schmoeckel E, Wuerstlein R, Harbeck N, Ditsch N, Jeschke U, Friese K, Kolben TM. The role of E-Cadherin expression in primary site of breast cancer. Arch Gynecol Obstet 2021;305:913-920. [PMID: 34510244 PMCID: PMC8967771 DOI: 10.1007/s00404-021-06198-1] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/13/2021] [Accepted: 08/17/2021] [Indexed: 12/15/2022]

Affiliation(s)

Nora Karsten Department of Obstetrics and Gynaecology, Breast Center and CCCLMU, LMU University Hospital, Marchioninistr. 15, 81377, Munich, Germany
Thomas Kolben Department of Obstetrics and Gynaecology, Breast Center and CCCLMU, LMU University Hospital, Marchioninistr. 15, 81377, Munich, Germany
Sven Mahner Department of Obstetrics and Gynaecology, Breast Center and CCCLMU, LMU University Hospital, Marchioninistr. 15, 81377, Munich, Germany
Susanne Beyer Department of Obstetrics and Gynaecology, Breast Center and CCCLMU, LMU University Hospital, Marchioninistr. 15, 81377, Munich, Germany
Sarah Meister Department of Obstetrics and Gynaecology, Breast Center and CCCLMU, LMU University Hospital, Marchioninistr. 15, 81377, Munich, Germany
Christina Kuhn Department of Gynaecology and Obstetrics, University Hospital, Stenglinstr. 2, 86156, Augsburg, Germany
Elisa Schmoeckel Department of Pathology, LMU Munich, Marchioninistr. 27, 81377, Munich, Germany
Rachel Wuerstlein Department of Obstetrics and Gynaecology, Breast Center and CCCLMU, LMU University Hospital, Marchioninistr. 15, 81377, Munich, Germany
Nadia Harbeck Department of Obstetrics and Gynaecology, Breast Center and CCCLMU, LMU University Hospital, Marchioninistr. 15, 81377, Munich, Germany
Nina Ditsch Department of Gynaecology and Obstetrics, University Hospital, Stenglinstr. 2, 86156, Augsburg, Germany
Udo Jeschke Department of Obstetrics and Gynaecology, Breast Center and CCCLMU, LMU University Hospital, Marchioninistr. 15, 81377, Munich, Germany. .,Department of Gynaecology and Obstetrics, University Hospital, Stenglinstr. 2, 86156, Augsburg, Germany.
Klaus Friese Department of Oncology, Hospital Bad Trissl, Bad-Trissl-Straße 73, 83080, Oberaudorf, Germany
Theresa Maria Kolben Department of Obstetrics and Gynaecology, Breast Center and CCCLMU, LMU University Hospital, Marchioninistr. 15, 81377, Munich, Germany

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Shi M, Whorton AE, Sekulovski N, Paquet M, MacLean JA, Song Y, Van Dyke T, Hayashi K. Inactivation of TRP53, PTEN, RB1, and/or CDH1 in the ovarian surface epithelium induces ovarian cancer transformation and metastasis. Biol Reprod 2021;102:1055-1064. [PMID: 31930396 DOI: 10.1093/biolre/ioaa008] [Citation(s) in RCA: 18] [Impact Index Per Article: 4.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/26/2019] [Revised: 12/24/2019] [Accepted: 01/09/2020] [Indexed: 01/03/2023] Open

Partial EMT in head and neck cancer biology: a spectrum instead of a switch. Oncogene 2021;40:5049-5065. [PMID: 34239045 PMCID: PMC8934590 DOI: 10.1038/s41388-021-01868-5] [Citation(s) in RCA: 73] [Impact Index Per Article: 18.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/06/2021] [Revised: 05/03/2021] [Accepted: 05/25/2021] [Indexed: 12/14/2022]

The genomic architecture of metastasis in breast cancer: focus on mechanistic aspects, signalling pathways and therapeutic strategies. Med Oncol 2021;38:95. [PMID: 34268641 DOI: 10.1007/s12032-021-01547-1] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/08/2021] [Accepted: 07/03/2021] [Indexed: 12/13/2022]

Abstract

Breast cancer is a multifactorial, heterogeneous disease and the second most frequent cancer amongst women worldwide. Metastasis is one of the most leading causes of death in these patients. Early-stage or locally advanced breast cancer is limited to the breast or nearby lymph nodes. When breast cancer spreads to farther tissues/organs from its original site, it is referred to as metastatic or stage IV breast cancer. Normal breast development is regulated by specific genes and signalling pathways controlling cell proliferation, cell death, cell differentiation and cell motility. Dysregulation of genes involved in various signalling pathways not only leads to the formation of primary tumour but also to the metastasis as well. The metastatic cascade is represented by a multi-step process including invasion of the local tumour cell followed by its entry into the vasculature, exit of malignant cells from the circulation and ultimately their colonization at the distant sites. These stages are referred to as formation of primary tumour, angiogenesis, invasion, intravasation and extravasation, respectively. The major sites of metastasis of breast cancer are the lymph nodes, bone, brain and lung. Only about 28% five-year survival rate has been reported for stage IV breast cancer. Metastasis is a serious concern for breast cancer and therefore, various therapeutic strategies such as tyrosine kinase inhibitors have been developed to target specific dysregulated genes and various signalling pathways involved in different steps of metastasis. In addition, other therapies like hyperbaric oxygen therapy, RNA interference and CRISPR/Cas9 are also being explored as novel strategies to cure the stage IV/metastatic breast cancer. Therefore, the current review has been compiled with an aim to evaluate the genetic basis of stage IV breast cancer with a focus on the molecular mechanisms. In addition, the therapeutic strategies targeting these dysregulated genes involved in various signalling pathways have also been discussed. Genome editing technologies that can target specific genes in the affected areas by making knock-in and knock-out alternations and thereby bring significant treatment outcomes in breast cancer have also been summarized.

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Algaber A, Madhi R, Hawez A, Rönnow CF, Rahman M. Targeting FHL2-E-cadherin axis by miR-340-5p attenuates colon cancer cell migration and invasion. Oncol Lett 2021;22:637. [PMID: 34295384 PMCID: PMC8273858 DOI: 10.3892/ol.2021.12898] [Citation(s) in RCA: 9] [Impact Index Per Article: 2.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/25/2020] [Accepted: 03/25/2021] [Indexed: 01/04/2023] Open

Abstract

Convincing data has suggested that four and a half LIM domain 2 protein (FHL2) serves a key function in cancer cell metastasis and that microRNA (miR)-340-5p can regulate cancer cell migration. The current study hypothesized that targeting FHL2 expression by miR-340-5p in colon cancer may attenuate colon cancer cell migration and invasion. FHL2 expression was therefore assessed in colon cancer microarray datasets using Qlucore omics explorer as well as in HT-29 and AZ-97 colon cancer cell lines via reverse transcription-quantitative PCR (RT-qPCR). Colon cancer cell migration and invasion were evaluated in the presence of miR-340-5p mimic, mimic control or mimic with a target site blocker. Confocal microscopy and RT-qPCR were subsequently performed to assess FHL2, E-cadherin (E-cad) protein and mRNA expression in colon cancer cells. Microarray dataset analysis revealed that FHL2 expression was lower in primary colon cancer cells compared with normal colonic mucosa. It was revealed that the expression of miR-340-5p and FHL2 were inversely related in serum-grown and low-serum conditions in HT-29 and AZ-97 cells. Short-time serum exposure to low-serum grown cells induced FHL2 expression. Transfection of HT-29 cells with miR-340-5p mimic not only decreased serum-induced expression of FHL2 but also decreased cancer cell migration and invasion. Bioinformatics analysis revealed that FHL2 mRNA had one putative binding site for miR-340-5p at the 3-untranslated region. Blocking of the target site using a specific blocker reverted miR-340-5p mimic-induced inhibition of FHL2 expression and cancer cell migration and invasion. Confocal microscopy confirmed that the reduction of FHL2 expression by miR-340-5p mimic also reversed serum-induced E-cad disruption and that the target site blocker abrogated the effect of miR-340-5p. The current results suggested that miR-340-5p could be used to antagonize colon cancer cell metastasis by targeting the FHL2-E-cad axis.

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Zhang A, Aslam H, Sharma N, Warmflash A, Fakhouri WD. Conservation of Epithelial-to-Mesenchymal Transition Process in Neural Crest Cells and Metastatic Cancer. Cells Tissues Organs 2021;210:151-172. [PMID: 34218225 DOI: 10.1159/000516466] [Citation(s) in RCA: 4] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/18/2020] [Accepted: 04/12/2021] [Indexed: 11/19/2022] Open

Erman A, Kamenšek U, Dragin Jerman U, Pavlin M, Čemažar M, Veranič P, Romih R. How Cancer Cells Invade Bladder Epithelium and Form Tumors: The Mouse Bladder Tumor Model as a Model of Tumor Recurrence in Patients. Int J Mol Sci 2021;22:6328. [PMID: 34199232 PMCID: PMC8232005 DOI: 10.3390/ijms22126328] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/28/2021] [Revised: 06/07/2021] [Accepted: 06/08/2021] [Indexed: 12/03/2022] Open

Korpal M, Yelamanchi R, Durga CK, Bharadwaj M, Kambalimath C. Immunohistochemical E-cadherin Expression and Response to Chemotherapy in Breast Cancer Subjects. Indian J Surg 2021;83:421-426. [DOI: 10.1007/s12262-020-02576-2] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/11/2020] [Accepted: 08/15/2020] [Indexed: 11/24/2022] Open