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LncRNA LINC00525 suppresses p21 expression via mRNA decay and triplex-mediated changes in chromatin structure in lung adenocarcinoma

ABSTRACT: LncRNA LINC00525 suppresses p21 expression via mRNA decay and triplex-mediated changes in chromatin structure in lung adenocarcinoma Our findings demonstrate that LINC00525 promote lung adenocarcinoma progression by reducing the transcription and stability of p21 mRNA in concert with EZH2 and RBMS2, which highlights the importance of LINC00525 acting as a potential therapeutic target of LUAD.

ORGANISM(S): Homo sapiens

PROVIDER: GSE171460 | GEO | 2021/04/06

REPOSITORIES: GEO

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LncRNA LINC00525 suppresses p21 expression via mRNA decay and triplex-mediated changes in chromatin structure in lung adenocarcinoma

Project description:LncRNA LINC00525 suppresses p21 expression via mRNA decay and triplex-mediated changes in chromatin structure in lung adenocarcinoma

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The LncRNA Fendrr Regulates Lung Development via its Triplex Forming Site the Expression of Fibrosis Genes

Project description:Long non-coding RNAs are a very versatile class of molecules that have important roles in regulating a cells function, including regulating other genes on the transcriptional level. One of these mechanisms is that RNA can directly interact with DNA by recruiting additional components such as proteins to these sites via a RNA:dsDNA triplex formation. We genetically deleted the triplex forming sequence from the lncRNA Fendrr in mice and find that this FendrrBox is partially required for Fendrr function. we We find that the loss of the triplex forming site in developing lungs causes a dysregulation of gene programs, associated with lung fibrosis. Deregulated genes that contain a FendrrBox binding element in their promoter are regulated by Wnt signaling, together with Fendrr, implicating that Fendrr acts in concert with Wnt signaling to regulate lung fibrosis.

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Multileveled reduction of p21 expression by Linc-ASEN represses cellular senescence [ChIRP-seq]

Project description:Long noncoding RNAs regulating diverse cellular processes implicate in many diseases. Here, we report the identification of a novel long intergenic noncoding RNA, Linc-ASEN, expressed in prematurely senescent cells, that associates with UPF1 and represses cellular senescence by reducing p21 production transcriptionally and post-transcriptionally. The Linc-ASEN-UPF1 complex suppressed p21 transcription by recruiting Polycomb Repressive Complex 1 (PRC1) and PRC2 to the p21 locus, and thereby preventing binding of the transcriptional activator p53 on the p21 promoter. Moreover, the Linc-ASEN-UPF1 complex repressed p21 expression post-transcriptionally by lowering p21 mRNA stability in association with DCP1A. Accordingly, Linc-ASEN levels were found inversely correlated with p21 mRNA levels in tumor tissues from patient-derived xenograft mice, in various human cancer tissues, and in aged mice tissues. Our studies reveal that Linc-ASEN prevents cellular senescence by reducing the transcription and stability of p21 mRNA in concert with UPF1, and suggest that Linc-ASEN might be a potential therapeutic target in processes influenced by senescence, including cancer.

2019-09-24 | GSE128396 | GEO

Multileveled reduction of p21 expression by Linc-ASEN represses cellular senescence [RNA-seq]

2019-09-24 | GSE128395 | GEO

Multileveled reduction of p21 expression by Linc-ASEN represses cellular senescence [ChIP-seq]

2019-09-24 | GSE128397 | GEO

Integrative multi-omic analysis of the SWI/SNF complex defines a new clinical subgroup of lung adenocarcinoma patients

Project description:Mammalian SWI/SNF complexes are ATP-dependent chromatin remodelers composed of varying combinations of subunits that, together, fine-tune transcriptional regulation and genome integrity. SWI/SNF complex subunits have been identified as major targets of mutations in several tumor types suggesting a relevant role in tumorigenesis. However, there is a lack of comprehensive studies of the whole SWI/SNF complex in lung adenocarcinoma (LUAD). Here, we combined genomic, transcriptomic, and proteomic approaches to identify which SWI/SNF subunits are present in lung cells, as well as their mutational status, mRNA levels, and protein levels in LUAD. For these purposes, we combined data from LUAD primary tumors, normal lung and LUAD cell lines, and external LUAD data from The Cancer Genome Atlas. Importantly, we found that mutations in the SWI/SNF complex in LUAD not only present a high incidence but we also observed that only the mutational status of the SWI/SNF complex and not the mutations in any of the top ten LUAD driver genes is associated with poorer overall survival in LUAD patients. Furthermore, we showed that the expression of the SWI/SNF complex in LUAD suffers an overall repression that cannot be explained exclusively by genetic alterations. Based on our findings, we propose that SWI/SNF-mutant LUAD tumors should be considered as a distinct subgroup with practical applications in the prognosis and follow-up of LUAD patients.

2022-04-01 | PXD017397 | Pride

Expression data of sham and p21-overexpressed MLE-12 cells

Project description:We report that p21 expression was increased in the alveolar epithelial type 2 cells (AEC2s) in a time dependent manner following multiple bleomycin induced pulmonary fibrosis (PF). The AEC2s with the elevated expression of p21 exhibited cell senescence and lost the ability of self-renewal and differentiation. Evaluation of mRNA profiles in sham and p21-adenovirus treated MLE-12 cells is helpful to analyze the changes of lung alveolar epithelial cells after p21 deposition.

2022-02-01 | GSE166198 | GEO

RNAseq of combined LUAD and SCLC tumors to look at gene expression changes

Project description:For in-depth characterization of neuroendocrine transformation, we analyzed clinical specimens consisting of combined lung adenocarcinoma (LUAD)/small cell lung carcinoma (SCLC) histology exhibiting clear spatial separation. Microdissection was performed for RNA sequencing.

2021-06-03 | E-MTAB-10399 | biostudies-arrayexpress

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