CRISPR screen reveals SOX2 as a critical regulator of CD133 and cellular stress response in glioblastoma

Glioblastoma (GBM) remains a formidable challenge in clinical settings due to limited treatments available. The surface protein CD133 marks glioblastoma stem cells (GSCs), cells capable of overcoming therapeutic pressures and correlate with more aggressiveness tumor phenotypes. In this study, we employed a CRISPR-Cas9 functional screen to deconvolute CD133 dynamics in tumors. This led us to establish that SOX2 is a key player in controlling the PROM1 gene, which in turn influences how cells react to stress factors, including those induced by chemoradiation treatment. The discoveries in this study shed light on the complex web of mechanisms that control the survival and resistance of GSCs, offering promising new avenues for targeting and potentially overcoming therapy resistance.

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Publication Details

Journal
Scientific Reports
Published
2025-10-16
DOI
https://doi.org/10.1038/s41598-025-20183-7
Primary Topic
RNA Research and Splicing
Type
article
Field-Weighted Citation Impact
0.00

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article

CRISPR screen reveals SOX2 as a critical regulator of CD133 and cellular stress response in glioblastoma

Sheila Kumari Singh, Rajeev Vibhakar, Muhammad Vaseem Shaikh, Chitra Venugopal et al.
Scientific Reports
RNA Research and Splicing
article

CRISPR screen reveals SOX2 as a critical regulator of CD133 and cellular stress response in glioblastoma

Sheila Kumari Singh, Rajeev Vibhakar, Muhammad Vaseem Shaikh, Chitra Venugopal, Etienne Danis, Stefan Custers, Chirayu Chokshi, Petar Miletic, Kevin R. Brown, Jason Moffat, Neil Savage
article en

Abstract

Glioblastoma (GBM) remains a formidable challenge in clinical settings due to limited treatments available. The surface protein CD133 marks glioblastoma stem cells (GSCs), cells capable of overcoming therapeutic pressures and correlate with more aggressiveness tumor phenotypes. In this study, we employed a CRISPR-Cas9 functional screen to deconvolute CD133 dynamics in tumors. This led us to establish that SOX2 is a key player in controlling the PROM1 gene, which in turn influences how cells react to stress factors, including those induced by chemoradiation treatment. The discoveries in this study shed light on the complex web of mechanisms that control the survival and resistance of GSCs, offering promising new avenues for targeting and potentially overcoming therapy resistance.

Scientific ReportsVol. 15(1)
University of Toronto (CA), Juravinski Cancer Centre (CA), McMaster University Medical Centre (CA), Hospital for Sick Children (CA), University of Colorado Cancer Center (US), University of Colorado Anschutz Medical Campus (US), University of Colorado Denver (US), McMaster University (CA)
GlaxoSmithKline, McMaster University, University of Toronto, Mitacs, Hospital for Sick Children
Openalex Percentile: Top 74%
RNA Research and Splicing
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