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Homo sapiens

ABSTRACT: The Estrogen receptor alpha regulated NEAT1 long non-coding RNA promotes prostate cancer progression [ChIP-Seq]

OTHER RELATED OMICS DATASETS IN: GSE43986GSE43988

PROVIDER: PRJNA188302 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR658528.fastq.gz	Fastqsanger.gz
	SRR658529.fastq.gz	Fastqsanger.gz
	SRR658530.fastq.gz	Fastqsanger.gz
	SRR658531.fastq.gz	Fastqsanger.gz
	SRR658532.fastq.gz	Fastqsanger.gz

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Project description:The Estrogen receptor alpha regulated NEAT1 long non-coding RNA promotes prostate cancer progression

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The Estrogen receptor alpha regulated NEAT1 long non-coding RNA promotes prostate cancer progression [RNA-Seq]

Project description:The Estrogen receptor alpha regulated NEAT1 long non-coding RNA promotes prostate cancer progression [RNA-Seq]

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The Estrogen receptor alpha regulated NEAT1 long non-coding RNA promotes prostate cancer progression [ChIP-Seq]

Project description:Prostate glands predominantly exhibit androgen dependence, but increasing evidence suggests that estrogen receptor signaling is involved in its development and pathogenesis. By integrating ChIP sequencing for estrogen receptor alpha (ERα) with transcriptome sequencing data from prostate cancer samples, we found ERα to significantly influence the noncoding transcriptome in prostate cancer. We identified one such long noncoding RNA, NEAT1, to play an important role in prostate cancer progression through direct regulation of transcription of its target genes. NEAT1, in an ERα dependent manner, promotes prostate tumorigenesis by interacting with and modulating chromatin state at promoters of prostate cancer specific signature genes. NEAT1 expression is positively correlated with PSMA in prostate adenocarcinoma and with B3GAT1 in neuroendocrine prostate cancer. This study identifies NEAT1 as a novel biomarker or therapeutic target in prostate cancer and also suggests that co-targeting ERα and androgen receptor (AR) may be effective for a subset of patients with advanced prostate cancer and with NEAT1 overexpression.

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NEAT1 promotes genome stability via m6A methylation-dependent regulation of CHD4

Project description:Long non-coding (lnc)RNA emerge as regulators of genome stability. The nuclear enriched abundant transcript 1 (NEAT1) is overexpressed in many tumours and responsive to genotoxic stress. However, the mechanism that links NEAT1 to DNA damage response (DDR) is unclear. Here, we investigate the expression, modification levels, localization and structure of NEAT1 in response to DNA double-strand breaks (DSBs). DNA damage increases the levels and N6-methyladenosine (m6A) marks on NEAT1, which promotes alterations in NEAT1 structure, accumulation of hyper-methylated NEAT1 at promoter-associated DSBs and DSB foci formation. The depletion of NEAT1 delays DSB signalling and elevates DNA damage. The genome-protective role of NEAT1 is mediated by the RNA methyltransferase 3 (METTL3) and involves the release of the chromodomain helicase DNA binding protein 4 (CHD4) from NEAT1 to fine-tune histone deacetylation, which links NEAT1 to DDR.

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