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SOX2 Binds to CD133 in Glioblastoma Stem Cells to Regulate Cellular Stress Pathways Underlying Treatment Resistance

ABSTRACT: SOX2 Binds to CD133 in Glioblastoma Stem Cells to Regulate Cellular Stress Pathways Underlying Treatment Resistance

PROVIDER: PRJNA1273897 | ENA |

REPOSITORIES: ENA

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SOX2 Binds to CD133 in Glioblastoma Stem Cells to Regulate Cellular Stress Pathways Underlying Treatment Resistance

Project description:Glioblastoma (GBM) remains a formidable challenge in clinical settings due to limited treatments available for patients. The surface protein CD133 identifies glioblastoma stem cells (GSCs), cells capable of overcoming therapeutic pressures and correlate with more aggressive tumor phenotypes. In our study, we utilized a CRISPR-based genetic screen and Cleavage Under Targets and Release Using Nuclease (CUT&RUN) workflows to distinguish molecular differences between healthy neural stem cells (NSCs) and GSCs. This revealed heightened SOX2 expression directly binds to the PROM1 gene in GSCs, and upregulates genes associated with stress responses including those contributing to chemoradiation resistance. Our findings demonstrate the power of complementary genomic tools, CRISPR screens with CUT&RUN, to unravel complex gene regulatory networks. This integrated approach offers insights into overlapping fields of cancer biology and stem cell research.

2025-06-23 | GSE299313 | GEO

CRISPR Screen Reveals SOX2 as a Critical Regulator of CD133 and Cellular Stress Response in Glioblastoma II

Project description:Glioblastoma (GBM) remains a formidable challenge in clinical settings due 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.

2025-06-17 | GSE299588 | GEO

The Sox2 transcription factor binds RNA

Project description:The Sox2 transcription factor binds RNA

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Transcriptome analysis of CD133 overexpressed U87MG glioblastoma cells

Project description:This study investigated the biological function of CD133 by ectopic expression of CD133 in U87MG cell line. Although CD133 is widely used as a cancer stem cell marker, there are a few studies that examined its own biological functions. While a number of loss-of-function studies about CD133 have shown that CD133 have effects on cancer progression, there are few gain-of-function studies about functions of CD133. Thus, we identified the potential function of CD133 by its overexpression in U87MG glioblastoma cell line. Though there were no significant changes in cell growth and sphere forming ability, elevated IL-1β and its downstream chemokines (CCL3, CXCL3, CXCL5) may function as chemoattractants which affect recruitment of Ly6G+ neutrophils surrounding necrotic regions in vivo and migration of neutrophil-like dHL-60 cells. Taken together, this results imply that CD133 can regulate IL-1β signaling, and promotes the environmental change.

2017-08-03 | GSE99385 | GEO

CRISPR Screen Reveals SOX2 as a Critical Regulator of CD133 and Cellular Stress Response in Glioblastoma

Project description:CRISPR Screen Reveals SOX2 as a Critical Regulator of CD133 and Cellular Stress Response in Glioblastoma

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Competitive binding of E3 ligases TRIM26 and WWP2 controls SOX2 in glioblastoma

Project description:The pluripotency transcription factor SOX2 is essential for the maintenance of glioblastoma stem cells (GSC), which drive tumor growth and treatment resistance.To understand how SOX2 is regulated in GSCs, we utilized a proteomic approach and identified the E3 ubiquitin ligase TRIM26 as a direct SOX2-interacting protein. Unexpectedly, we found TRIM26 depletion decreased SOX2 protein levels and increased SOX2 polyubiquitination in patient-derived GSCs, suggesting TRIM26 promotes SOX2 protein stability. Accordingly, TRIM26 knockdown reduced SOX2 transcriptional activity, self-renewal capacity, and in vivo tumorigenicity in multiple GSC lines. Mechanistically, we found TRIM26, via its C-terminal PRYSPRY domain, but independent of its RING domain, stabilizes SOX2 protein by directly inhibiting the interaction of SOX2 with WWP2, which we identify as a bona fide SOX2 E3 ligase in GSCs. Our work identifies E3 ligase competition as a critical mechanism of SOX2 regulation, with functional consequences for GSC identity and maintenance.

2021-11-04 | PXD028933 | Pride

CRISPR Screen Reveals SOX2 as a Critical Regulator of CD133 and Cellular Stress Response in Glioblastoma II

Project description:CRISPR Screen Reveals SOX2 as a Critical Regulator of CD133 and Cellular Stress Response in Glioblastoma II

| PRJNA1275024 | ENA

The Sox2 transcription factor binds RNA

Project description:A subset of transcription factors is proposed to form functional interactions with RNA to facilitate proper regulation of gene expression. Sox2, a critical transcription factor for maintenance of pluripotency and neurogenesis, is found associated with several lncRNAs, although it is unknown whether these interactions are direct or via other proteins. We demonstrate that human Sox2 interacts directly with one of these lncRNAs with high affinity through its HMG DNA-binding domain. Furthermore, rather than interacting with a single high affinity site, Sox2 binds regions of dsRNA in a non-sequence specific fashion. RNA binding is competitive with dsDNA, yet interaction with RNA is primarily electrostatically driven using a partially overlapping set of amino acids as that used for DNA binding. Finally, we use two distinct crosslinking techniques, formaldehyde and UV, with RNA immunoprecipitation (respectively, “fRIP” and “UVRIP”) of Sox2 in mouse embryonic stem cells to identify >1000 potential Sox2-RNA interacting partners with ~75% overlap between the two techniques. Together, these data reveal that Sox2 productively binds dsRNA with affinities rivaling ChIP-validated promoter DNA sites, suggesting that the transcriptome plays a significant role in regulation of gene expression by Sox2.

2020-03-16 | GSE142013 | GEO

CRISPR Screen Reveals SOX2 as a Critical Regulator of CD133 and Cellular Stress Response in Glioblastoma

Project description:Looking for transcriptional differences between CD133 positive brain tumour initiating cells and CD133 negative brain tumour initiating cells and normal neural stem cells.

2025-11-22 | GSE283717 | GEO

Elevating Sox2 levels deleteriously affects the growth of glioblastoma and medulloblastoma cells.

Project description:Induction of the transcription factor Sox2 from a doxycycline-inducible promoter in iSox2-DAOY medulloblastoma cells. Affymetrix microarrays were used to characterize the gene expression profile of iSox2-DAOY cells in the absence and presence of doxycycline. Human DAOY medulloblastoma cells were engineered to express epitope tagged Sox2 under the control of a doxycycline inducible promoter, to produce iSox2-DAOY cells. iSox2-DAOY cells were FACS sorted into CD133 low and high populations. The CD133 low population was cultured in the absence and presence of 0.5 Âµg/mL doxycycline for 24 hours. RNA was extracted from cells cultured without and with doxycycline, and was used for microarray analysis.

2012-08-25 | E-GEOD-36947 | biostudies-arrayexpress

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