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

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

PROVIDER: PRJNA1275024 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33943300.fastq.gz	Fastqsanger.gz
	SRR33943291.fastq.gz	Fastqsanger.gz
	SRR33943292.fastq.gz	Fastqsanger.gz
	SRR33943293.fastq.gz	Fastqsanger.gz
	SRR33943294.fastq.gz	Fastqsanger.gz

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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

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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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.

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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

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.

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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.

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Activation of a SOX2-dependent transcriptional regulatory circuit drives glioblastoma.

Project description:Overexpression of the transcription factor SRY-related box 2 (SOX2) is characteristic of Glioblastoma (GBM), yet its regulatory network in vivo is poorly understood. Using a human orthotopic tumor model of GBM for ChIP-Seq analysis, we mapped the SOX2 cistrome. Integrative analysis of SOX2 cistrome and GBM transcriptome data identified two transcription factors, oligodendrocyte lineage transcription factor 2 (OLIG2) and zinc finger E-box binding homeobox 1 (ZEB1) as critical SOX2 targets. Their expression is strongly correlated with SOX2 expression in clinical GBM specimens, and all three proteins are frequently co-expressed in primary Glioblastoma cells, even in the setting of EGFR intratumoral heterogeneity. Sox2, Olig2, and Zeb1 expression is activated by the oncogene EGFRvIII in a murine glioma model, and we demonstrate that co-expression of these transcription factors transforms tumor suppressor deficient astrocytes in the absence of an upstream oncogene and that the resulting tumors exhibit the major histopathological features of GBM.

2017-01-24 | GSE58345 | 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.

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CD133+ vs. CD133- cells in GBML8, a primary glioblastoma tumorsphere culture

Project description:CD133+ and CD133- cells were FACS islated from GBML8 cells to find gene signatures upregulated in cancer stem cells

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