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Homo sapiens

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

PROVIDER: PRJNA374919 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5260593.fastq.gz	Fastqsanger.gz
	SRR5260594.fastq.gz	Fastqsanger.gz

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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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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. Current findings have identified a novel E2F1 associated cistrome and transcriptome that is associated with RB loss in PCa. In order to determine the contribution of chromatin accessibility to alterations in E2F1 activity, ATAC-Seq was performed.

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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.

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

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RB1 loss promotes a noncanonical activator function of LSD1 and sensitizes castration-resistant prostate cancer to LSD1 inhibition [RNA-seq]

Project description:Genomic loss of RB1 is a common alteration in castration-resistant prostate cancer (CRPC) and is associated with poor patient outcomes. RB1-loss is also a driver event that promotes the neuroendocrine transdifferentiation of prostate cancer (PCa). The loss of Rb protein disrupts the Rb-E2F repressor complex and thus hyperactivates E2F transcription activators. While the impact of RB1-loss on PCa progression and linage plasticity has been previously studied, the underline mechanisms remain unclear. Using an integrated cistromic and transcriptomic analysis, we have characterized Rb activities in multiple CRPC models by identifying Rb directly regulated genes and revealed that Rb has distinct binding sites and targets in TP53-mutated CRPC. Significantly, we show that RB1-loss promotes the noncanonical activator function of LSD1/KDM1A, which stabilizes chromatin binding of E2F1, and hence sensitizes CRPC tumor to the LSD1 inhibitor treatment. These results provide new molecular insights of Rb activity in PCa progression and suggest LSD1 as a potential therapeutic target in CRPC with RB1-loss.

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RB1 loss promotes a noncanonical activator function of LSD1 and sensitizes castration-resistant prostate cancer to LSD1 inhibition [ChIP-seq]

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RSK1-driven TRIM28-E2F1 feedback loop promotes castration-resistant prostate cancer progression

Project description:Castration-resistant prostate cancer (CRPC) marks the advanced and lethal stage of prostate cancer (PCa). TRIM28, also known as KAP1, is a transcriptional regulator recently shown to promote CRPC cell proliferation and xenograft tumor growth. Nonetheless, knowledge gaps persist regarding the mechanisms underlying TRIM28 upregulation in CRPC as well as the genomic targets regulated by TRIM28. Here, we report that TRIM28 is a novel E2F1-target in CRPC. Using an integrated genomic approach, we have demonstrated that TRIM28 forms a positive feedback loop to promote the transcription activation and genomic function of E2F1 independent of Rb status. Furthermore, we identified RSK1 as a kinase that directly phosphorylates TRIM28 at S473, and as such, RSK1 drives the TRIM28-E2F1 feedback loop. Accordingly, pS473-TRIM28 promotes CRPC progression, which is mitigated by RSK inhibition. In summary, our study reveals a critical role of the RSK1–TRIM28–E2F1 axis in CRPC progression, which may be exploited as a vulnerability in treating Rb-deficient CRPC.

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2018-05-16 | GSE103871 | GEO

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Project description:Biological implications of healthy- and tumor-specific ERα cistromes in endometrial tumors have largely been understudied. Moreover, the functional impact of non-coding somatic variants has commonly been underexplored and remained elusive. This study is aimed to provide functional interpretation of non-coding somatic variants associated with tumor-specific ERα cistrome. Integrating the ChIP-seq analyses with the whole genome sequencing from the set of metastatic endometrial tumors and matched controls we observed that tumor-specific ERα cistrome is enriched for somatic variants. Additionally, H3K27Ac Hi-ChIP in cancer cell lines identified potential target genes of tumor-specific enhancers and coincident variants. We aim to employ CRISPR to identify tumor-specific ERα enhancers and target genes critical for estrogen-driven proliferation of endometrial cancer-cell lines. Through multidimensional omics data integration, our study is specifically geared to shed new lights on the molecular mechanisms of endometrial cancer development and progression and the functional impact of non-coding somatic mutations.

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