Published online Jun 24, 2024. doi: 10.5306/wjco.v15.i6.687
Revised: April 27, 2024
Accepted: May 20, 2024
Published online: June 24, 2024
Processing time: 173 Days and 7.5 Hours
Glioma is one of the most common primary intracranial tumors, characterized by invasive growth and poor prognosis. Actin cytoskeletal rearrangement is an essential event in tumor cell migration. Scinderin (SCIN), an actin severing and capping protein that regulates the actin cytoskeleton, is involved in the proliferation and migration of certain cancer cells. However, its biological role and molecular mechanism in glioma remain unclear. Lin et al explored the role and mechanism of SCIN in gliomas. The results showed that SCIN mechanically affected cytoskeleton remodeling and inhibited the formation of lamellipodia via RhoA/FAK signaling pathway. This study identifies the cancer-promoting role of SCIN and provides a potential therapeutic target for SCIN in glioma treatment.
Core Tip: The role of scinderin (SCIN) in cancer progression has been studied, but its role in glioma remains unknown. Lin et al found that the expression level of SCIN mRNA was positively correlated with the tumor grade of glioma. SCIN affected cytoskeletal remodeling and inhibited lamellipodia formation through RhoA/FAK signaling pathway, thereby facilitating the migration and invasion of glioma cells.
