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P63/p73 maintain cancer stem cells in a quasi-mesenchymal state and drive metastatic colonization via EGFR signaling [ATAC-Seq]

ABSTRACT: p63/p73 are master transcriptional regulators of ITGB4-hi cancer stem cells and are required to maintain CSCs in a quasi-mesenchymal state and for metastatic colonization

ORGANISM(S): Homo sapiens

PROVIDER: GSE172405 | GEO | 2022/11/22

REPOSITORIES: GEO

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p63/p73 maintain cancer stem cells in a quasi-mesenchymal state and drive metastatic colonization via EGFR signaling [ChIP-Seq]

Project description:p63/p73 are master transcriptional regulators of ITGB4-hi cancer stem cells and are required to maintain CSCs in a quasi-mesenchymal state and for metastatic colonization

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p63/p73 maintain cancer stem cells in a quasi-mesenchymal state and drive metastatic colonization via EGFR signaling

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p63/p73 maintain cancer stem cells in a quasi-mesenchymal state and drive metastatic colonization via EGFR signaling [ATAC-Seq]

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miRNA array after p63 knock down in human squamous cell carcinoma

Project description:A central challenge in human cancer therapy is the identification of pathways that control tumor cell survival and chemosensitivity in the absence of functional p53. The p53-related transcription factors p63 and p73 exhibit distinct, p53-independent roles in development and cancer: p73 promotes genome stability and mediates chemosensitivity, while p63 largely lacks these p53-like functions and instead promotes proliferation and cell survival. Here, we identify a new and physiologically important mechanism of p63/p73 cross-talk which governs the balance between pro-survival and pro-apoptotic programs in both human and murine squamous cell carcinoma. Through comprehensive profiling of p63-regulated microRNAs (miRs), we identified a subset which target p73 for inhibition, including miR-193a-5p, a direct endogenous transcriptional target repressed by p63 and activated by pro-apoptotic p73 isoforms in both normal cells and tumor cells in vivo. Consequently, chemotherapy treatment causes p63/p73-dependent induction of this miR, thereby limiting chemosensitivity due to miR-mediated feedback control of p73. We demonstrate that interrupting this feedback by inhibiting miR-193a suppresses tumor cell viability and induces dramatic chemosensitivity both in vitro and in vivo. Thus, we have identified a direct, miR-dependent regulatory circuit mediating inducible chemoresistance, whose inhibition provides a new therapeutic opportunity in p53-deficient tumors. Knockdown of endogenous p63 by p63-directed or control lentiviral shRNA in JHU-029 human SCC cells at 48h, in duplicate experiments. Array analysis showing the fold-change and direction of change for all miRs regulated > 1.5-fold in p63-ablated versus control samples

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p63/p73 maintain cancer stem cells in a quasi-mesenchymal state and drive metastatic colonization via EGFR signaling

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-11-22 | GSE172407 | GEO

miRNA array after p63 knock down in human squamous cell carcinoma

2010-11-23 | GSE25524 | GEO