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Chip-Seq analysis of Sox2 protein genome-wide DNA binding sites in glioma cancer cells

ABSTRACT: We report here our results of the genome wide target identification of SOX2 in GBM cells by ChIP-seq analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE23795 | GEO | 2011/01/10

SECONDARY ACCESSION(S): PRJNA133145

REPOSITORIES: GEO

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Chip-Seq analysis of Sox2 protein genome-wide DNA binding sites in glioma cancer cells

Project description:We report here our results of the genome wide target identification of SOX2 in GBM cells by ChIP-seq analysis. Identification of Sox2 DNA binding site in glioma cancer cells

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IQGAP3 bridges matrix stiffness with glioma stem cell maintenance and radioresistance by stabilizing SOX2

Project description:Drivers of therapeutic resistance in cancer include evolution of tumor cell heterogeneity and the tumor microenvironment (TME). Here, we found that increased matrix stiffness promotes radioresistance in glioblastoma (GBM) and maintains the tumor cell hierarchy. Differential gene expression revealed that stiff matrices induced expression of IQGAP3 (IQ Motif Containing GTPase Activating Protein 3) specifically in GBM stem cells (GSCs). IQGAP3 promoted GSC self-renewal and survival upon radiation treatment through binding and stabilization of the core stem cell transcription factor, SOX2. Targeting IQGAP3 reduced SOX2 protein levels in vitro and in vivo, increasing GSC radiosensitivity and inhibiting tumor growth. Structure-function drug screening of FDA-approved agents blocking IQGAP3 binding to SOX2 identified trimetrexate as a brain penetrant pharmacologic disruptor of IQGAP3 function in radioresistance, sensitizing GSCs to radiotherapy. Our results identify molecular underpinnings for biomechanical promotion of cancer stem cell maintenance and therapeutic resistance, informing a therapeutic strategy to augment efficacy of radiotherapy.

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IQGAP3 bridges matrix stiffness with glioma stem cell maintenance and radioresistance by stabilizing SOX2

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Pioneer activity distinguishes activating from non-activating SOX2 binding sites

Project description:Genome-wide transcriptional activity involves the binding of many transcription factors to thousands of sites in the genome. Determining which sites are directly driving transcription remains a challenge. Here we use acute protein depletion of the pioneer transcription factor SOX2 to establish its functionality in maintaining chromatin accessibility. We show that thousands of accessible sites are lost within an hour of protein depletion, indicating rapid turnover of these sites in the absence of pioneer factors. To understand the relationship with transcription we performed nascent transcription analysis and found that open chromatin sites that are maintained by SOX2 are highly predictive of gene expression, in contrast to all other SOX2 binding sites. We use CRISPR-Cas9 genome editing in the Klf2 locus to functionally validate a predicted regulatory element. We conclude that the regulatory activity of SOX2 is exerted largely at sites where it maintains accessibility and that other binding sites are largely dispensable for gene regulation.

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Pupylation sites on protein Sox2

Project description:As a test for the effectiveness of SPIDER with RNA-protein pairs, We used Sox2 and specific biotin-DNA and biotin-RNA to validate the efficiency of SPIDER capturing protein-nucleic acid interaction. Pupylation sites on Sox2 after SPIDER assay was identified by LC-MS/MS analysis, by searching for an additional mass of ~243 Da, which represents the three C-terminal residues of Pup, i. e., GGE, that covalently binds to adjacent lysine by pupylation. ）

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