The landscape of enhancer transcription in prostate cancer [RNA-Seq]
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ABSTRACT:
PROVIDER: PRJNA912767 | ENA |
REPOSITORIES: ENA
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Project description:The landscape of enhancer transcription in prostate cancer
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Project description:High-fat diet and obesity are high risk factors for colorectal cancer. The underlying mechanism is still unclear. Environmental factors alter the epigenome to affect gene expression thus the phenotype. In response to external stimuli, the cis-regulatory regions, especially enhancer loci, are key elements for regulating selective gene expression. We thus explored the effects of high-fat diet and the accompanying obesity on gene expression and the enhancer landscape in colon epithelium. High-fat diet exposed binding sites of transcription factors downstream of signaling pathways important in the initiation and progression of colon cancer. Meantime, colon-specific enhancers were lost rendering the cells potential for dedifferentiation. The alteration at enhancer regions drives a specific transcription program promoting colon cancer progression. The comprehensive interrogation of enhancer changes by high-fat diet in colon epithelium provides a number of insights into the underlying biology of high-fat diet and obesity in increasing colon cancer risk, and provides potential therapeutic targets to treat obese colon cancer patients. We measured gene expression in colon epithelium from wild type mice and NAG-1 (non-steroidal anti-inflammatory drug (NSAID)-activated gene-1) transgenic mice fed either a 10% fat diet (LF) or a 60% fat diet (HF) for 20 weeks, using Agilent Whole Mouse Genome 4x44 multiplex format oligo arrays (014868) (Agilent Technologies) following the Agilent 1-color microarray-based gene expression analysis protocol. The ChIP-seq component of the study is included in GSE46748.
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Project description:Amplification of the androgen receptor (AR) locus is the most frequent alteration in metastatic treatment resistant prostate cancer. Recently it was discovered that an enhancer of the AR is co-amplified with the AR gene body and contributes to increased AR transcription and resistance to androgen deprivation therapy. However, the mechanism of enhancer activation in advanced disease is unknown. Here, we used functional genetic screening to identify transcription factors that bind to the AR enhancer and are required for enhancer mediated AR transcription. We validated binding of the transcription factors, HOXB13, GATA2, and TFAP2C in patient derived xenografts and demonstrated differential effects on features associated with active chromatin state including H3K27ac, DNA accessibility, and enhancer-promoter interaction frequency. Interestingly, the AR enhancer belongs to a set of regulatory elements that requires HOXB13 to maintain FOXA1 binding, uncovering a novel role for HOXB13 in castration-resistant prostate cancer. This work provides a framework to functionally identify trans-acting factors required for activation of disease related noncoding regulatory elements.
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Project description:Amplification of the androgen receptor (AR) locus is the most frequent alteration in metastatic treatment resistant prostate cancer. Recently it was discovered that an enhancer of the AR is co-amplified with the AR gene body and contributes to increased AR transcription and resistance to androgen deprivation therapy. However, the mechanism of enhancer activation in advanced disease is unknown. Here, we used functional genetic screening to identify transcription factors that bind to the AR enhancer and are required for enhancer mediated AR transcription. We validated binding of the transcription factors, HOXB13, GATA2, and TFAP2C in patient derived xenografts and demonstrated differential effects on features associated with active chromatin state including H3K27ac, DNA accessibility, and enhancer-promoter interaction frequency. Interestingly, the AR enhancer belongs to a set of regulatory elements that requires HOXB13 to maintain FOXA1 binding, uncovering a novel role for HOXB13 in castration-resistant prostate cancer. This work provides a framework to functionally identify trans-acting factors required for activation of disease related noncoding regulatory elements.
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Project description:Amplification of the androgen receptor (AR) locus is the most frequent alteration in metastatic treatment resistant prostate cancer. Recently it was discovered that an enhancer of the AR is co-amplified with the AR gene body and contributes to increased AR transcription and resistance to androgen deprivation therapy. However, the mechanism of enhancer activation in advanced disease is unknown. Here, we used functional genetic screening to identify transcription factors that bind to the AR enhancer and are required for enhancer mediated AR transcription. We validated binding of the transcription factors, HOXB13, GATA2, and TFAP2C in patient derived xenografts and demonstrated differential effects on features associated with active chromatin state including H3K27ac, DNA accessibility, and enhancer-promoter interaction frequency. Interestingly, the AR enhancer belongs to a set of regulatory elements that requires HOXB13 to maintain FOXA1 binding, uncovering a novel role for HOXB13 in castration-resistant prostate cancer. This work provides a framework to functionally identify trans-acting factors required for activation of disease related noncoding regulatory elements.
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