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
Abstract
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 migration and invasion in several cancers.
AIM
To investigate the role and mechanism of SCIN in glioma.
METHODS
The expression and clinical significance of SCIN in glioma were analyzed based on public databases. SCIN expression was examined using real-time quantitative polymerase chain reaction and Western blotting. Gene silencing was performed using short hairpin RNA transfection. Cell viability, migration, and invasion were assessed using cell counting kit 8 assay, wound healing, and Matrigel invasion assays, respectively. F-actin cytoskeleton organization was assessed using F-actin staining.
RESULTS
SCIN expression was significantly elevated in glioma, and high levels of SCIN were associated with advanced tumor grade and wild-type isocitrate dehydrogenase. Furthermore, SCIN-deficient cells exhibited decreased proliferation, migration, and invasion in U87 and U251 cells. Moreover, knockdown of SCIN inhibited the RhoA/focal adhesion kinase (FAK) signaling to promote F-actin depolymerization in U87 and U251 cells.
CONCLUSION
SCIN modulates the actin cytoskeleton via activating RhoA/FAK signaling, thereby promoting the migration and invasion of glioma cells. This study identified the cancer-promoting effect of SCIN and provided a potential therapeutic target for the treatment of glioma.
Core Tip: Actin dynamics-related protein scinderin (SCIN) was found to be significantly upregulated in glioma, and high SCIN expression was associated with advanced tumor grade and wild-type isocitrate dehydrogenase. Furthermore, silenced-SCIN cells exhibited decreased proliferation, migration, and invasion. Besides, knockdown of SCIN inhibited RhoA/focal adhesion kinase signaling to promote F-actin depolymerization in glioma cells.
