RBMS1 interference inhibits malignant progression of glioblastoma cells and promotes ferroptosis.

Discov Oncol

Department of Neurosurgery, Affiliated Hospital of Shaoxing University, No. 999 Zhongxing Southern Road, Shaoxing, 312000, Zhejiang, China.

Published: October 2024

AI Article Synopsis

  • Glioblastoma (GBM) is an aggressive brain tumor with poor survival rates, and RBMS1 is a protein that may influence its progression.
  • This study utilized various laboratory techniques to analyze RBMS1 expression and its effects on GBM cell behaviors, like proliferation, apoptosis, and invasion.
  • The findings indicated that reducing RBMS1 levels decreased GBM cell malignancy and promoted ferroptosis, a type of cell death, suggesting RBMS1 plays a significant role in GBM progression.

Article 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.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11469991PMC
http://dx.doi.org/10.1007/s12672-024-01430-1DOI Listing

Publication Analysis

Top Keywords

rbms1 expression
12
rbms1
9
malignant progression
8
western blot
8
cell proliferation
8
cell apoptosis
8
migration invasion
8
expression upregulated
8
upregulated gbm
8
detected
7

Similar Publications

RBMS1 interference inhibits malignant progression of glioblastoma cells and promotes ferroptosis.

Discov Oncol

October 2024

Department of Neurosurgery, Affiliated Hospital of Shaoxing University, No. 999 Zhongxing Southern Road, Shaoxing, 312000, Zhejiang, China.

Article Synopsis
  • Glioblastoma (GBM) is an aggressive brain tumor with poor survival rates, and RBMS1 is a protein that may influence its progression.
  • This study utilized various laboratory techniques to analyze RBMS1 expression and its effects on GBM cell behaviors, like proliferation, apoptosis, and invasion.
  • The findings indicated that reducing RBMS1 levels decreased GBM cell malignancy and promoted ferroptosis, a type of cell death, suggesting RBMS1 plays a significant role in GBM progression.
View Article and Find Full Text PDF

RBMS1 reflects a distinct microenvironment and promotes tumor progression in ocular melanoma.

Exp Eye Res

September 2024

Department of Ophthalmology, Ninth People's Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, 200011, PR China; Shanghai Key Laboratory of Orbital Diseases and Ocular Oncology, Shanghai, 200011, PR China. Electronic address:

Ocular melanoma, including uveal melanoma (UM) and conjunctival melanoma (CM), is the most common ocular cancer among adults with a high rate of recurrence and poor prognosis. Loss of epigenetic homeostasis disturbed gene expression patterns, resulting in oncogenesis. Herein, we comprehensively analyzed the DNA methylation, transcriptome profiles, and corresponding clinical information of UM patients through multiple machine-learning algorithms, finding that a methylation-driven gene RBMS1 was correlated with poor clinical outcomes of UM patients.

View Article and Find Full Text PDF

Increased ANKRD1 Levels in Early Senescence Mediated by RBMS1-Elicited mRNA Stabilization.

Mol Cell Biol

May 2024

Laboratory of Genetics and Genomics, National Institute on Aging Intramural Research Program, National Institutes of Health, Baltimore, Maryland, USA.

Cellular senescence is a dynamic biological process triggered by sublethal cell damage and driven by specific changes in gene expression programs. We recently identified ANKRD1 (ankyrin repeat domain 1) as a protein strongly elevated after triggering senescence in fibroblasts. Here, we set out to investigate the mechanisms driving the elevated production of ANKRD1 in the early stages of senescence.

View Article and Find Full Text PDF

Background: Osteoarthritis (OA) is the most prevalent and commonly chronic joint disease that frequently develops among the elderly population. It is not just a single tissue that is affected, but rather a pathology involving the entire joint. Among them, synovitis is a key pathological change in OA.

View Article and Find Full Text PDF
Article Synopsis
  • The study investigates how long-range projection neurons in the cerebral cortex regulate RNA localization and translation in their growth cones, which are the tips of growing axons.
  • By comparing the transcriptomes of two types of projection neurons, it uncovers both unique and shared mechanisms that relate to neurodevelopmental and psychiatric disorders.
  • The research identifies specific RNA-binding proteins, like CPEB4 and RBMS1, that play crucial roles in RNA regulation, which is essential for proper circuit formation and has implications for understanding related disorders.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!