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Oncogenic properties of NEAT1 in prostate cancer cells depend on the CDC5L-AGRN transcriptional regulation circuit

ABSTRACT: Silencing NEAT1 in prostate cancer cells repressed the transcriptional activity of CDC5L, and RNA-seq and further analyses revealed a handful of potential targets of CDC5L regulated by NEAT1 expression. We have established the requirement of the CDC5L-AGRN circuit for the essential oncogenic role of NEAT1 in prostate cancer cells. Here we provide processed raw counts files.

ORGANISM(S): Homo sapiens

PROVIDER: GSE114959 | GEO | 2018/06/01

REPOSITORIES: GEO

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Oncogenic properties of NEAT1 in prostate cancer cells depend on the CDC5L-AGRN transcriptional regulation circuit

Project description:Oncogenic properties of NEAT1 in prostate cancer cells depend on the CDC5L-AGRN transcriptional regulation circuit

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

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Project description:We identified the gene cell division cycle 5-like protein (CDC5L), whose knockdown induced SG formation in the absence of any cellular stress. Moreover, lower protein levels of CDC5L increased mRNA and protein levels of PERK. Through ChIP-PCR, we found that CDC5L regulated transcription by directly binding to PERK promoter.To further clarify the biological function of CDC5L as a transcriptional repressor, we expressed CDC5L-HA in the HeLa cell line, used HA antibodies for chromatin immunoprecipitation, and obtained the promoters to which CDC5L protein directly binds, and performed ChIP-seq analysis.

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Project description:Stress granules (SGs) are membraneless protein condensates that form in the cytoplasm of a cell upon exposure to cellular stressors. Here, we identified the gene cell division cycle 5-like protein (CDC5L), whose knockdown induced SG formation in the absence of any cellular stress. Moreover, lower protein levels of CDC5L increased mRNA and protein levels of PERK. In order to identify the regulation on the overall cellular transcriptome, especially stress-related genes, after CDC5L knockdown, we used siRNA to knockdown CDC5L and performed RNA-seq in the HeLa cell line.

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Project description:CDC5L in HeLa cell lines

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Project description:The lncRNA NEAT1 is overexpressed in multiple myeloma (MM) plasma cells and plays a key role in MM pathogenesis. NEAT1 is involved in ceRNA network in several cancers; however, data in MM are virtually absent. This study identified a NEAT1-driven ceRNA network involving 96 miRNAs and 40 target genes, selected as concurrently downregulated in NEAT1-KD AMO1 cells and upregulated in NEAT1-overexpressing AMO1 cells (AMO1-OVX). The co-expression of NEAT1 and the targets was validated in MM patients (GSE116294, GSE13591, GSE6477, CoMMpass), and in NEAT1-KD NCI-H929, LP1, and KMS27 cell lines, showing for all targets a consistent downregulation, resembling that of NEAT1. The functional implication of the ceRNA network was explored by functional enrichment analyses of the 40 targets, identifying 78 significant gene sets, 17 of which found significantly enriched by GSEA analysis in at least one experimental condition among NEAT1-KD LP1, NCI-H929, and KMS27 cells, AMO1-OVX cells, or the extreme quartiles of NEAT1 expression in the CoMMpass dataset. Noteworthy, the cell cycle gene set was validated in 5 out of 6 conditions tested, suggesting that in MM the impact of NEAT1 upregulation on the cell cycle, experimentally demonstrated in our earlier publications, may be attributable, at least partially, to ceRNA mechanisms.

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RNA-Seq results of cervical spinal cords from NEAT1-KO; hSOD1G93A mice, compared to NEAT1-WT; hSOD1G93A

Project description:Transcriptional changes of NEAT1-KO; hSOD1G93A mice and NEAT1-WT; hSOD1G93A mice were compared. RNA-seq gene expression analysis revealed that differentially expressed genes were associated with protein folding as biological process.

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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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