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RBMS1 interference inhibits malignant progression of glioblastoma cells and promotes ferroptosis.
- Source :
- Discover Oncology; 10/11/2024, Vol. 15 Issue 1, p1-13, 13p
- Publication Year :
- 2024
-
Abstract
- Background: Glioblastoma (GBM) is a brain tumor characterized by the highest malignancy and the poorest prognoses. RNA binding motif single strand interacting protein 1 (RBMS1) has been implicated to be involved in various cancer progression. This study was conceived to explore the role and the mechanism of RBMS1 in GBM. Materials: RT-qPCR and western blot were used to evaluate RBMS1 expression and examine the transfection efficiency of sh-RBMS1. Cell proliferation was detected using CCK-8 assay and colony formation assay while cell apoptosis was detected with flow cytometry. Cell migration and invasion were detected with wound healing and transwell assay. The activities of MMP2 and MMP9 were detected using gelatin zymography. Western blot was used to measure proliferation-, apoptosis-, ferroptosis- and EMT-related proteins. Lipid peroxidation was detected with TBARS Assay Kit and lipid ROS was detected with a BODIPY 581/591 C11 kit. The total iron level was detected using corresponding assay kits. Results: According to GEPIA database, RBMS1 expression was upregulated in GBM and the present study found that RBMS1 expression was upregulated in GBM cells. After interfering RBMS1, GBM cell proliferation, migration, invasion and EMT process were inhibited while cell apoptosis and ferroptosis were promoted. However, ferroptosis inhibitor Fer-1 partially counteracted the protective effects of RBMS1 knockdown on GBM. Conclusion: Collectively, this study revealed that RBMS1 silence inhibited the malignant progression of GBM possibly through ferroptosis. [ABSTRACT FROM AUTHOR]
- Subjects :
- BRAIN tumors
CELL migration
GLIOBLASTOMA multiforme
WOUND healing
CELL proliferation
Subjects
Details
- Language :
- English
- ISSN :
- 27306011
- Volume :
- 15
- Issue :
- 1
- Database :
- Complementary Index
- Journal :
- Discover Oncology
- Publication Type :
- Academic Journal
- Accession number :
- 180235896
- Full Text :
- https://doi.org/10.1007/s12672-024-01430-1