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DBC1 promotes metastatic castration-resistant prostate cancer by enhancing the stability and activity of HSF1 [RNA-seq]

ABSTRACT: DBC1 promotes metastatic castration-resistant prostate cancer by enhancing the stability and activity of HSF1 [RNA-seq]

PROVIDER: PRJNA1156586 | ENA |

REPOSITORIES: ENA

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DBC1 promotes metastatic castration-resistant prostate cancer by enhancing the stability and activity of HSF1 [ChIP-seq]

Project description:Heat shock factor 1 (HSF1) is a key stress-protective transcription factor that is exploited by various cancers to promote cancer cell survival, therapy resistance, and metastasis. Metastatic castration-resistant prostate cancer (mCRPC) is the leading cause of cancer-related death in men worldwide, and mCRPC progression is associated with increased dependence on HSF1. However, mechanisms underlying HSF1 stabilization and persistent activation in metastatic malignancies remain unclear. Here we show that the HSF1-driven transcriptional program and its genome occupancy in mCRPC cells are distinct from those of CRPC cells. HSF1 is highly activated and required for the metastatic potential of mCRPC cells. Moreover, we report DBC1 as a critical regulator of HSF1 stability and activity in mCRPC cells. DBC1 is required for genome-wide chromatin occupancy and target gene expression of HSF1. Mechanistically, DBC1 enhances DYRK2/PKA-mediated HSF1 phosphorylation at S320/S326 and inhibits CHIP-mediated HSF1 ubiquitination, thereby stabilizing and activating HSF1. Importantly, DBC1 loss suppresses growth and metastasis of mCRPC cells, and high DBC1 expression correlates with poor outcomes in patients with mCRPC. Our results highlight the critical role of DBC1 as a key HSF1 coregulator in mCRPC progression and provide insights into regulatory mechanisms of HSF1 stability and activity in advanced and metastatic cancers.

2025-09-02 | GSE276302 | GEO

DBC1 promotes metastatic castration-resistant prostate cancer by enhancing the stability and activity of HSF1 [RNA-seq]

2025-09-02 | GSE276301 | GEO

DBC1 promotes metastatic castration-resistant prostate cancer by enhancing the stability and activity of HSF1 [ChIP-seq]

Project description:DBC1 promotes metastatic castration-resistant prostate cancer by enhancing the stability and activity of HSF1 [ChIP-seq]

| PRJNA1156585 | ENA

DBC1 regulates p53 stability via inhibition of CBP-dependent p53 polyubiquitination

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.

2019-11-13 | PXD012673 | Pride

Gene expression analysis of DBC1 KO B cells

Project description:DBC1 KO B cells were either unstimulated, activated with anti-IgM, anti-CD40 of LPS for 4 hours. Genes differentially expressed in DBC1 KO B cells were compared to WT B cells. RNA was collected from unstimulated for stimulated B cells, and gene expression between WT and DBC1 KO B cells were compared

2014-09-04 | E-GEOD-61029 | biostudies-arrayexpress

Gene expression analysis of DBC1 KO B cells

Project description:DBC1 KO B cells were either unstimulated, activated with anti-IgM, anti-CD40 of LPS for 4 hours. Genes differentially expressed in DBC1 KO B cells were compared to WT B cells.

2014-09-04 | GSE61029 | GEO

DBC1 is a positive regulator of enhancer epigenomic writers KMT2D and p300.

Project description:Genome-wide maps of DBC1, KMT2D, and p300 in SW480 WT and DBC1 KO cells

2022-08-17 | GSE202478 | GEO

Effect of DBC1/CCAR2 knockout on global gene expression in SW480 cells

2015-12-31 | GSE65841 | GEO

Effect of DBC1/CCAR2 knockout on global gene expression in SW480 cells

Project description:Deleted in breast cancer (DBC1; also known as CCAR2) is a coactivator for nuclear receptors (NRs) and other transcription factors as well as a negative regulator of epigenetic modifiers such as deacetylases SIRT1 and HDAC3. We performed genome-wide gene expression analysis in wild-type and DBC1 knockout SW480 cells to investigate global gene expression changes induced by DBC1 knockout. Total RNAs were isolated from SW480 wild-type and DBC1 knockout cells using the RNeasy mini kit (Qiagen). The integrity of RNA was analyzed using an Agilent 2100 Bioanalyzer. Three independent biological replicates were assayed for each sample. The microarrays were performed following the Affymetrix standard protocol.

2015-12-31 | E-GEOD-65841 | biostudies-arrayexpress

Effect of DBC1/CCAR2 depletion on global gene expression in MDA-MB-231 cells

Project description:Deleted in breast cancer (DBC1; also known as CCAR2) is a coactivator for nuclear receptors (NRs) as well as a negative regulator of epigenetic modifiers such as deacetylases SIRT1 and HDAC3. We performed genome-wide gene expression analysis in control (shNS) and DBC1-depleted (shDBC1) MDA-MD-231 cells to investigate global gene expression changes induced by depletion of DBC1

2015-01-31 | GSE54707 | GEO

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