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Updated: Oct 7, 2025

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Reduced RBPMS Levels Promote Cell Proliferation and Decrease Cisplatin Sensitivity in Ovarian Cancer Cells.

Robert J Rabelo-Fernández1,2, Ginette S Santiago-Sánchez1,3, Rohit K Sharma1

  • 1University of Puerto Rico Comprehensive Cancer Center, San Juan, PR 00935, USA.

International Journal of Molecular Sciences
|January 11, 2022
PubMed
Summary
This summary is machine-generated.

The RNA binding protein with multiple splicing (RBPMS) acts as a tumor suppressor in ovarian cancer. Lower RBPMS levels correlate with increased tumor growth, invasiveness, and cisplatin resistance, suggesting RBPMS as a potential therapeutic target.

Keywords:
CRISPRRNA binding protein with multiple splicingcisplatin resistanceovarian cancertumor suppressor gene

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Ovarian cancer frequently develops resistance to chemotherapy, particularly cisplatin, a major cause of mortality.
  • The RNA binding protein with multiple splicing (RBPMS) is implicated in RNA regulation but its role in ovarian cancer remains largely unknown.
  • Understanding mechanisms of chemotherapy resistance is crucial for improving patient outcomes.

Purpose of the Study:

  • To investigate the biological function of RBPMS in ovarian cancer.
  • To determine the relationship between RBPMS expression and patient survival and cisplatin sensitivity.
  • To identify downstream targets of RBPMS that could serve as biomarkers.

Main Methods:

  • Bioinformatic analysis of public databases (e.g., KM plotter).
  • Immunohistochemical analysis of RBPMS expression in ovarian cancer tissues.
  • CRISPR-mediated RBPMS knockout in OVCAR3 cells, followed by cell growth, invasion, and sensitivity assays.
  • RNA sequencing and proteomic analysis to identify RBPMS downstream effectors.
  • Senescence assays (β-galactosidase staining).

Main Results:

  • High RBPMS levels in ovarian cancer patients correlate with longer survival.
  • Ovarian cancer tissues exhibit lower RBPMS expression compared to normal tissues.
  • RBPMS knockout in OVCAR3 cells leads to increased proliferation, invasiveness, and cisplatin resistance.
  • RBPMS knockdown induces senescence in ovarian cancer cells.
  • RNAseq and proteomic analyses identified downstream targets involved in tumor microenvironment modulation, oncogenesis, and cell integrity.

Conclusions:

  • RBPMS functions as a tumor suppressor gene in ovarian cancer.
  • Reduced RBPMS expression promotes cisplatin resistance and aggressive tumor behavior.
  • RBPMS and its downstream effectors represent potential prognostic and therapeutic biomarkers for ovarian cancer.