RTT NEAT1
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ABSTRACT:
PROVIDER: PRJEB74772 | ENA |
REPOSITORIES: ENA
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Project description:The long noncoding RNA (lncRNA) Nuclear Enriched Abundant Transcript 1 (NEAT1) is a lncRNA involved in a variety of human cancers and diseases. The human NEAT1 gene produces two distinct isoforms, NEAT1 Long and NEAT1 Short, through alternative 3’ end formation. NEAT1 Long is an essential factor for nuclear paraspeckle formation, while the role of NEAT1 Short is poorly understood. Previous studies have often failed to distinctly detect the two NEAT1 isoforms and reported controversial NEAT1 dysregulation. Moreover, the molecular mechanisms which underlie the dysregulation of NEAT1 isoforms and their functional importance in tumorigenesis remain poorly characterized. We investigated whether usage of the proximal polyadenylation site (PAS) within the NEAT1 transcript is regulated to govern the biogenesis of NEAT1 isoforms in human glioma cells. We found differential dysregulation of NEAT1 isoforms in patient-derived human glioblastoma multiforme (GBM) stem cells. We further show deletion of the NEAT1 PAS reduced NEAT1 Short and increased NEAT1 Long. We identified the RNA binding protein QKI, a risk factor for glioma, facilitates the utilization of the NEAT1 PAS. We present evidence indicating the imbalance of NEAT1 isoforms correlates with transcriptomic pathway changes. We propose QKI-5 regulates NEAT1 isoform biogenesis through modulating the NEAT1 PAS in human glioma cells.
2024-10-01 | GSE262598 | GEO
Project description:p53 is a transcriptional activator that induces myriad target genes. However, those p53-inducible genes most critical for tumor suppression remain elusive. Here, we identify Neat1, a ncRNA constituent of paraspeckles, as a p53 target gene induced by mouse and human p53 in different cell types and by diverse stress signals. Using fibroblasts derived from Neat1-/- mice, we examine the functional role of Neat1 in the p53 pathway. We find that Neat1 is dispensable for cell-cycle arrest and apoptosis in response to genotoxic stress, but plays a crucial role in suppressing transformation in response to oncogenic signals. To determine the effects of Neat1 deficiency on cells, we used E1A;HRasV12-expressing wild-type and Neat1-/- mouse embryonic fibroblasts (MEFs) for RNA-sequencing analysis. This analysis revealed that Neat1 deficiency impacts the regulatory networks involved in nervous system development and axon guidance programs, as well as genes of the SWI/SNF complex and components of the pancreas development network. These findings suggest that the ability of Neat1 to globally regulate gene expression, with effects on diverse transcriptional programs, provides a potential mechanism for how Neat1 acts to suppress transformation and tumor initiation.
2017-07-27 | GSE100098 | GEO
Project description:Long non-coding (lnc)RNA emerge as regulators of genome stability. The nuclear enriched abundant transcript 1 (NEAT1) locus encodes two lncRNA isoforms that modulate gene expression, growth and proliferation in mammals. Interestingly, NEAT1 transcripts are overexpressed in many tumours and induced by DNA damage, suggesting a genome-protective function. However, the precise role of NEAT1 in the 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) induced by the topoisomerase-II inhibitor etoposide or the locus-specific endonuclease AsiSI. We find that induction of DSBs increases both the levels and N6-methyladenosine (m6A) marks on NEAT1, which promotes alterations in NEAT1 secondary structure and accumulation of hyper-methylated NEAT1 at a subset of promoter-associated DSBs to facilitate efficient DSB signalling. The depletion of NEAT1, in turn, delays the response to DSBs and triggers elevated DNA damage. The genome-protective role of NEAT1 is mediated by the RNA methyltransferase 3 (METTL3) and involves spreading of the chromodomain helicase DNA binding protein 4 (CHD4) upon release from NEAT1. Together, we describe a novel RNA-dependent DDR pathway that couples NEAT1 to the recognition and repair of DSBs.
2024-09-17 | GSE256233 | GEO
Project description:Long non-coding (lnc)RNA emerge as regulators of genome stability. The abundant nuclear enriched transcript 1 (NEAT1) locus encodes two lncRNA isoforms that modulate gene expression, growth and proliferation in mammals. Interestingly, NEAT1 transcripts are overexpressed in many tumours and induced by DNA damage, suggesting a genome-protective function. However, the precise role of NEAT1 in the 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) induced by the topoisomerase-II inhibitor etoposide or the locus-specific endonuclease AsiSI. We find that induction of DSBs increases both the levels and N6-methyladenosine (m6A) marks on NEAT1, which promotes alterations in NEAT1 secondary structure and accumulation of hyper-methylated NEAT1 at a subset of promoter-associated DSBs to facilitate efficient DSB signalling. The depletion of NEAT1, in turn, delays the response to DSBs and triggers elevated DNA damage. The genome-protective role of NEAT1 is mediated by the RNA methyltransferase 3 (METTL3) and involves spreading of the chromodomain helicase DNA binding protein 4 (CHD4) upon release from NEAT1. Together, we describe a novel RNA-dependent DDR pathway that couples NEAT1 to the recognition and repair of DSBs.
2024-09-16 | GSE255342 | GEO
Project description:Long non-coding (lnc)RNA emerge as regulators of genome stability. The abundant nuclear enriched transcript 1 (NEAT1) locus encodes two lncRNA isoforms that modulate gene expression, growth and proliferation in mammals. Interestingly, NEAT1 transcripts are overexpressed in many tumours and induced by DNA damage, suggesting a genome-protective function. However, the precise role of NEAT1 in the 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) induced by the topoisomerase-II inhibitor etoposide or the locus-specific endonuclease AsiSI. We find that induction of DSBs increases both the levels and N6-methyladenosine (m6A) marks on NEAT1, which promotes alterations in NEAT1 secondary structure and accumulation of hyper-methylated NEAT1 at a subset of promoter-associated DSBs to facilitate efficient DSB signalling. The depletion of NEAT1, in turn, delays the response to DSBs and triggers elevated DNA damage. The genome-protective role of NEAT1 is mediated by the RNA methyltransferase 3 (METTL3) and involves spreading of the chromodomain helicase DNA binding protein 4 (CHD4) upon release from NEAT1. Together, we describe a novel RNA-dependent DDR pathway that couples NEAT1 to the recognition and repair of DSBs.
2024-09-16 | GSE255341 | GEO
Project description:Long non-coding (lnc)RNA emerge as regulators of genome stability. The abundant nuclear enriched transcript 1 (NEAT1) locus encodes two lncRNA isoforms that modulate gene expression, growth and proliferation in mammals. Interestingly, NEAT1 transcripts are overexpressed in many tumours and induced by DNA damage, suggesting a genome-protective function. However, the precise role of NEAT1 in the 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) induced by the topoisomerase-II inhibitor etoposide or the locus-specific endonuclease AsiSI. We find that induction of DSBs increases both the levels and N6-methyladenosine (m6A) marks on NEAT1, which promotes alterations in NEAT1 secondary structure and accumulation of hyper-methylated NEAT1 at a subset of promoter-associated DSBs to facilitate efficient DSB signalling. The depletion of NEAT1, in turn, delays the response to DSBs and triggers elevated DNA damage. The genome-protective role of NEAT1 is mediated by the RNA methyltransferase 3 (METTL3) and involves spreading of the chromodomain helicase DNA binding protein 4 (CHD4) upon release from NEAT1. Together, we describe a novel RNA-dependent DDR pathway that couples NEAT1 to the recognition and repair of DSBs.
2024-09-16 | GSE255340 | GEO
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.
2024-09-16 | GSE273351 | GEO
Project description:Reduction of NEAT1 transcript associated with Cell type-specific differential expression. The Knockdown of NEAT1 in Huh7 cells modulated antiviral response and dengue virus replication via the RIG-I pathway. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different cells at two time points.
2023-01-11 | GSE209759 | GEO
Project description:Although thousands of long non-coding RNAs (lncRNAs) are localized in the nucleus, only a few dozen have been functionally characterized. We found that nuclear paraspeckle assembly transcript 1 (NEAT1), an essential lncRNA for the formation of nuclear body paraspeckles, is induced by poly I:C stimulation, resulting in excess formation of paraspeckles. Using microarray analysis, we investigated whether NEAT1 induction followed by excess formation of paraspeckles was involved in poly I:C-inducible gene expression. We want to know the NEAT1-regulated genes. To the end, HeLa TO cells with and without poly I:C stimulation and NEAT1-knock down cells with and without poly I:C stimulation and cells transfected with mock plasmid or Neat1v2 expression plasmid alone were used for RNA extraction and hybridization on Affymetrix microarrays.
2014-05-07 | E-GEOD-56936 | biostudies-arrayexpress
Project description:We investigated the role of NEAT1 knockdown on neuronal excitability in iPSC-derived neurons.
2017-01-26 | E-MTAB-3447 | biostudies-arrayexpress