Published online Jan 24, 2024. doi: 10.5306/wjco.v15.i1.32
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
Processing time: 136 Days and 21.9 Hours
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.
The biological role and molecular mechanism of SCIN in glioma remain unclear.
This study aims to investigate the role and mechanism of SCIN in glioma.
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.
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.
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.
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.
