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ScRNA gene expression of breast tumors with mutant p53 or mutant p53 deleted [scRNA-seq]

ABSTRACT: We conducted gene expression analysis from total tumor treated with AAV-Control or AAV-mut-p53 deleted in an acute setting.

ORGANISM(S): Mus musculus

PROVIDER: GSE213823 | GEO | 2024/01/01

REPOSITORIES: GEO

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Gene expression of breast tumors with mutant p53 or mutant p53 deleted [RNA-seq]

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RNA-seq and scRNA-seq gene expression of breast tumors with mutant p53 or mutant p53 deleted

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

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Project description:The control of p53 protein stability is critical to its tumor suppressor functions. The CREB Binding Protein (CBP) transcriptional coactivator co-operates with MDM2 to maintain normally low physiologic p53 levels in cells via an exclusively cytoplasmic ‘E4’ polyubiquitination activity. Utilizing mass spectrometry to identify nuclear and cytoplasmic CBP interacting proteins that regulate compartmentalized CBP E4 activity, we identified Deleted in Breast Cancer 1 (DBC1) as a stoichiometric CBP-interacting protein that negatively regulates CBP–dependent p53 polyubiquitination, stabilizes p53, and augments p53-dependent apoptosis. TCGA analysis demonstrated that solid tumors often retain wild type p53 alleles in conjunction with DBC1 loss, supporting the hypothesis that DBC1 is selected for disruption during carcinogenesis as a surrogate for p53 functional loss. As DBC1 maintains p53 stability in the nucleus where p53 exerts its tumor suppressive transcriptional function, replacement of DBC1 functionality in DBC1-deleted tumors might also enhance p53 function and chemosensitivity for therapeutic benefit.

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