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

OTHER RELATED OMICS DATASETS IN: GSE43986GSE43988

PROVIDER: PRJNA188299 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR658524_1.fastq.gz	Fastqsanger.gz
	SRR658524_2.fastq.gz	Fastqsanger.gz
	SRR658525_1.fastq.gz	Fastqsanger.gz
	SRR658525_2.fastq.gz	Fastqsanger.gz
	SRR658526_1.fastq.gz	Fastqsanger.gz

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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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Project description:The Estrogen receptor alpha regulated NEAT1 long non-coding RNA promotes prostate cancer progression [ChIP-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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Project description:The first aim of the study was to identify the genes regulated by the estrogen receptor alpha (ERa) in the normal mouse prostate, with and without the co-activation of the androgen receptor. The second objective was to decipher the changes in the estrogen and androgen responses in a tumoral context from prostate cancer-developping mice.

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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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Project description:Breast cancer is one of the most prevalent cancers in women worldwide. Through the regulation of many coding and non-coding target genes, estrogen (E2 or 17b-estradiol) and its nuclear receptor ERα play important roles in breast cancer development and progression. Despite intensive studies on estrogen-regulated coding genes over the past decades, molecular mechanisms underlying estrogen-regulated non-coding RNAs in breast cancer remain to be elucidated. Here, we performed extensive epigenomic studies including GRO-seq and ATAC-seq, and identified genome-wide estrogen-regulated long non-coding RNAs (lncRNAs). Similar to the coding targets of ERα, the transcription of estrogen-regulated lncRNAs correlates with the activation status of ERα-bound enhancers, measured by eRNA production, chromatin accessibility, and the occupancy of the enhancer regulatory components including P300, MED1, and ARID1B. Our 3D chromatin architecture analyses suggest that lncRNAs and their neighboring E2-resonsive coding genes, exemplified by LINC00160 and RUNX1, might be regulated as a 3D structural unit resulted from enhancer-promoter interactions. Finally, we evaluated the expression levels of LINC00160 and RUNX1 in various types of breast cancer and found that their expression positively correlated with the survival rate in ER+ breast cancer patients, implying that the estrogen-regulated LINC00160 and its neighboring RUNX1 might represent potential biomarkers for ER+ breast cancers.

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