Lin X, Zhao Z, Sun SP, Liu W. Scinderin promotes glioma cell migration and invasion via remodeling actin cytoskeleton. World J Clin Oncol 2024; 15(1): 32-44 [PMID: 38292665 DOI: 10.5306/wjco.v15.i1.32]
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Clin Oncol. Jan 24, 2024; 15(1): 32-44 Published online Jan 24, 2024. doi: 10.5306/wjco.v15.i1.32
Scinderin promotes glioma cell migration and invasion via remodeling actin cytoskeleton
Xin Lin, Zhao Zhao, Shu-Peng Sun, Wei Liu
Xin Lin, Zhao Zhao, Shu-Peng Sun, Wei Liu, Department of Neurosurgery, Tianjin Huanhu Hospital, Tianjin 300000, China
Author contributions: Lin X designed the research study; Lin X, Zhao Z, Sun S, and Liu W performed the research; Zhao Z and Sun S contributed new reagents and analytic tools; Lin X analyzed the data and wrote the manuscript; All authors have read and approved the final manuscript.
Institutional review board statement: The study was reviewed and approved by the Institutional Review Board of Tianjin Huanhu Hospital.
Informed consent statement: All study participants or their legal guardians provided informed written consent about personal and medical data collection before study enrollment.
Conflict-of-interest statement: The authors have no relevant financial or non-financial interests to disclose.
Data sharing statement: The mRNA expression and clinical data of glioma analyzed during the current study are available on the GEPIA database (http://gepia.cancer-pku.cn/) and CGGA) database (http://www.cgga.org.cn/). The protein expression of glioma analyzed in this study is also available on the UALCAN database (https://ualcan.path.uab.edu/). Other datasets during and/or analyzed during the current study are available from the corresponding author upon reasonable request.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Received: September 8, 2023 Peer-review started: September 8, 2023 First decision: October 17, 2023 Revised: November 20, 2023 Accepted: December 19, 2023 Article in press: December 19, 2023 Published online: January 24, 2024
ARTICLE HIGHLIGHTS
Research background
Glioma is one of the most common intracranial tumors, characterized by invasive growth and poor prognosis. Actin cytoskeletal rearrangement is an essential event of tumor cell migration. The actin dynamics-related protein scinderin (SCIN) has been reported to be closely related to tumor cell mobility and invasion in several cancers.
Research motivation
The biological role and molecular mechanism of SCIN in glioma remain unclear.
Research objectives
This study aims to investigate the role and mechanism of SCIN in glioma.
Research methods
The expression and clinical significance of SCIN were analyzed in glioma based on public databases. Then, we utilized SCIN-specific short hairpin RNAs to knock down SCIN expression in glioma cell lines and observed the effects of SCIN silencing on the proliferative, migrative, and invasive abilities of glioma cells. Furthermore, the effect of SCIN silencing on the cytoskeleton of glioma cells was also investigated.
Research results
SCIN expression was significantly elevated in glioma, and high levels of SCIN were associated with advanced tumor grade and wild-type dehydrogenase. SCIN-deficient cells exhibited repressed proliferation, migration, and invasion in U87 and U251 cells. The knockdown of SCIN promotes F-actin depolymerization in U87 and U251 cells via inhibiting RhoA/FAK signaling.
Research conclusions
Our work illustrates a novel mechanism of SCIN-mediated glioma progression and suggests the possibility that SCIN might be a potential therapeutic target for glioma treatment.
Research perspectives
To explore SCIN as a biomarker for glioma diagnosis in more clinical samples. To investigate the potential anticancer value of SCIN as an intervention target in vivo.
