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Identification of the RB loss-induced transcriptome and E2F1 cistrome in prostate cancer

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE94959 | GEO | 2018/02/22

REPOSITORIES: GEO

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Identification of the RB loss-induced E2F1 cistrome in prostate cancer [ChIP-seq]

Project description:The retinoblastoma protein (RB) is preferentially lost in the progression to castrate resistant prostate cancer (CRPC). However, the alterations associated with such loss have been scantly described. The current study aims to provide molecular mechanisms underlying Rb loss-driven CRPC phenotypes.

2018-02-22 | GSE94958 | GEO

Identification of the RB loss-induced transcriptome and E2F1 cistrome in prostate cancer

Project description:Identification of the RB loss-induced transcriptome and E2F1 cistrome in prostate cancer

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Comparison of the RB loss-induced E2F1 cistrome in hormone-therapy sensitive and castration-resistant prostate cancer [ChIP-seq]

Project description:These studies examine the consequence of RB loss on E2F1 function across prostate cancer progression.

2021-04-26 | GSE154191 | GEO

Identification of the RB loss-induced transcriptome in prostate cancer [RNA]

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RB Loss Promotes Prostate Cancer Metastasis.

Project description:RB loss occurs commonly in neoplasia but its contributions to advanced cancer have not been assessed directly. Here we show that RB loss in multiple murine models of cancer produces a prometastatic phenotype. Gene expression analyses showed that regulation of the cell motility receptor RHAMM by the RB/E2F pathway was critical for epithelial-mesenchymal transition, motility, and invasion by cancer cells. Genetic modulation or pharmacologic inhibition of RHAMM activity was sufficient and necessary for metastatic phenotypes induced by RB loss in prostate cancer. Mechanistic studies in this setting established that RHAMM stabilized F-actin polymerization by controlling ROCK signaling. Collectively, our findings show how RB loss drives metastatic capacity and highlight RHAMM as a candidate therapeutic target for treating advanced prostate cancer. Cancer Res; 77(4); 982-95. ©2016 AACR.

| S-EPMC5700768 | biostudies-literature

Identification of ZBTB7A cistrome and transcriptome profiles in VCaP prostate cancer cells

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

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Comparison of the RB loss-induced E2F1 cistrome in hormone-therapy sensitive and castration-resistant prostate cancer [ChIP-seq]

Project description:Comparison of the RB loss-induced E2F1 cistrome in hormone-therapy sensitive and castration-resistant prostate cancer [ChIP-seq]

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Comparison of the RB loss-induced transcrptiome in hormone-therapy sensitive and castration-resistant prostate cancer

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

2021-04-26 | GSE154192 | GEO

CEBPD reverses RB/E2F1-mediated gene repression and participates in HMDB-induced apoptosis of cancer cells.

Project description:PURPOSE:Recent evidence indicates that a tumor suppressor gene CEBPD (CCAAT/enhancer-binding protein delta) is downregulated in many cancers including cervical cancer, which provides a therapeutic potential associated with its reactivation. However, little is known for CEBPD activators and the effect of reactivation of CEBPD transcription upon anticancer drug treatment. In this study, we identified a novel CEBPD activator, 1-(2-hydroxy-5-methylphenyl)-3-phenyl-1,3-propanedione (HMDB). The purpose of this study is to characterize the mechanism of HMDB-induced CEBPD activation and its potential effect in cancer therapy. EXPERIMENTAL DESIGN:Methylation-specific PCR assay, reporter assay, and chromatin immunoprecipitation (ChIP) assay were performed to dissect the signaling pathway of HMDB-induced CEBPD transcription. Furthermore, a consequence of HMDB-induced CEBPD expression was linked with E2F1 and retinoblastoma (RB), which discloses the scenario of CEBPD, E2F1, and RB bindings and transcriptional regulation on the promoters of proapoptotic genes, PPARG2 and GADD153. Finally, the anticancer effect of HMDB was examined in xenograft mice. RESULTS:We demonstrate that CEBPD plays an essential role in HMDB-mediated apoptosis of cancer cells. HMDB up-regulates CEBPD transcription through the p38/CREB pathway, thus leading to transcriptional activation of PPARG2 and GADD153. Furthermore, increased level of CEBPD attenuates E2F1-induced cancer cell proliferation and partially rescues RB/E2F1-mediated repression of PPARG2 and GADD153 transcription. Moreover, HMDB treatment attenuates the growth of A431 xenografts in severe combined immunodeficient mice mice. CONCLUSIONS:These results clearly demonstrate that HMDB kills cancer cells through activation of CEBPD pathways and suggest that HMDB can serve as a superior chemotherapeutic agent with limited potential for adverse side effects.

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The RB-E2F1 pathway regulates autophagy.

Project description:Autophagy is a protective mechanism that renders cells viable in stressful conditions. Emerging evidence suggests that this cellular process is also a tumor suppressor pathway. Previous studies showed that cyclin-dependent kinase inhibitors (CDKI) induce autophagy. Whether retinoblastoma protein (RB), a key tumor suppressor and downstream target of CDKIs, induces autophagy is not clear. Here, we show that RB triggers autophagy and that the RB activators p16INK4a and p27/kip1 induce autophagy in an RB-dependent manner. RB binding to E2 transcription factor (E2F) is required for autophagy induction and E2F1 antagonizes RB-induced autophagy, leading to apoptosis. Downregulation of E2F1 in cells results in high levels of autophagy. Our findings indicate that RB induces autophagy by repressing E2F1 activity. We speculate that this newly discovered aspect of RB function is relevant to cancer development and therapy.

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