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MiRNA and lncRNA expression networks modulate Cell Cycle and DNA repair inhibition in senescent prostate cells. [miRNA-Seq]

ABSTRACT: miRNA and lncRNA expression networks modulate Cell Cycle and DNA repair inhibition in senescent prostate cells. [miRNA-Seq]

PROVIDER: PRJNA781968 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16988068.fastq.gz	Fastqsanger.gz
	SRR16988069.fastq.gz	Fastqsanger.gz
	SRR16988070.fastq.gz	Fastqsanger.gz
	SRR16988071.fastq.gz	Fastqsanger.gz

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miRNA and lncRNA expression networks modulate Cell Cycle and DNA repair inhibition in senescent prostate cells.

Project description:miRNA and lncRNA expression networks modulate Cell Cycle and DNA repair inhibition in senescent prostate cells.

| PRJNA781966 | ENA

miRNA and lncRNA expression networks modulate Cell Cycle and DNA repair inhibition in senescent prostate cells. [RNA-Seq]

Project description:miRNA and lncRNA expression networks modulate Cell Cycle and DNA repair inhibition in senescent prostate cells. [RNA-Seq]

| PRJNA781967 | ENA

miRNA and lncRNA expression networks modulate Cell Cycle and DNA repair inhibition in senescent prostate cells. [miRNA-Seq]

2022-03-03 | GSE189207 | GEO

miRNA and lncRNA expression networks modulate Cell Cycle and DNA repair inhibition in senescent prostate cells. [RNA-Seq]

2022-03-03 | GSE189208 | GEO

miRNA and lncRNA Expression Networks Modulate Cell Cycle and DNA Repair Inhibition in Senescent Prostate Cells.

Project description:Cellular senescence is a state of permanent growth arrest that arises once cells reach the limit of their proliferative capacity. It creates an inflammatory microenvironment favouring the initiation and progression of various age-related diseases, including prostate cancer. Non-coding RNAs (ncRNAs) have emerged as important regulators of cellular gene expression. Nonetheless, very little is known about the interplay of microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) and how deregulation of ncRNA networks promotes cellular senescence. To investigate this, human prostate epithelial cells were cultured through different passages until senescent, and their RNA was extracted and sequenced using RNA sequencing (RNAseq) and microRNA sequencing (miRNA-seq) miRNAseq. Differential expression (DE) gene analysis was performed to compare senescent and proliferating cells with Limma, miRNA-target interactions with multiMiR, lncRNA-target interactions using TCGA data and network evaluation with miRmapper. We found that miR-335-3p, miR-543 and the lncRNAs H19 and SMIM10L2A all play central roles in the regulation of cell cycle and DNA repair processes. Expression of most genes belonging to these pathways were down-regulated by senescence. Using the concept of network centrality, we determined the top 10 miRNAs and lncRNAs, with miR-335-3p and H19 identified as the biggest hubs for miRNAs and lncRNA respectively. These ncRNAs regulate key genes belonging to pathways involved in cell senescence and prostate cancer demonstrating their central role in these processes and opening the possibility for their use as biomarkers or therapeutic targets to mitigate against prostate ageing and carcinogenesis.

| S-EPMC8872619 | biostudies-literature

Cellular and functional characterization of aging-independent senescent-like cells that modulate tissue repair

Project description:Cellular and functional characterization of aging-independent senescent-like cells that modulate tissue repair

| PRJNA1067582 | ENA

miRNA and lncRNA expression networks modulate Cell Cycle and DNA repair inhibition in senescent prostate cells.

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-03-03 | GSE189209 | GEO

Cellular and functional characterization of aging-independent senescent-like cells that modulate tissue repair

Project description:Cells expressing features of cellular senescence, including upregulation of p21 and p16, appear transiently following tissue injury, yet the properties of these cells or how they contrast with age-induced senescent cells remains unclear. Using skeletal fracture as a model of acute injury, we identified rapidly-appearing senescent-like cells, marked by p21 expression, that negatively affected fracture healing. p21+ callus cells, which consisted predominantly of neutrophils and osteochondroprogenitors, existed as transient cells specific to injury and expressed high levels of senescence-associated factors known to impair bone formation and induce paracrine senescence. Targeted genetic clearance of p21+ cells suppressed senescence-associated signatures within the fracture callus and accelerated fracture healing. By contrast, p21+ cell clearance did not alter bone loss due to aging; conversely, p16+ cell clearance, known to alleviate skeletal aging, did not affect fracture healing. Together, our findings establish contextual roles of senescent/senescent-like cells that may be leveraged for therapeutic opportunities.

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Senescent cells suppress innate VSMC repair functions in atherosclerosis

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Accumulating DNA damage and insufficient DNA repair in senescent cells underlie persistent DNA damage signaling

Project description:Senescent cells are a major cause of organismal aging and a key target for anti-aging therapies. Persistent DNA damage signaling is a primary driver of the induction and maintenance of cellular senescence. However, many DNA damaging stimuli that induce senescence, such as irradiation or transient exposure to genotoxic drugs, are transient. The mechanisms underlying persistent damage signaling in senescent cells, and why senescent cells fail to repair damaged DNA, remain unknown. Here, we were able to assess the mechanisms underlying persistence of DNA damage and senescence maintenance by designing a precisely controllable senescence system that does not require potent stressors to induce senescence. We demonstrate that sustained mTORC1 signaling in senescent cells causes gradually accumulating DNA damage and an inflammatory response that maintains cell-cycle arrest. Markedly, activation of E2F transcription, which promotes expression of DNA repair proteins, can reverse accumulated DNA damage. Thus, persistent DNA damage signaling arises in senescent cells by uncoupling of mTORC1 and E2F signaling, whereby prolonged mTORC1 activity causes gradually increasing DNA damage that cannot be sufficiently repaired without induction of protective E2F target genes.

2023-06-01 | GSE153683 | GEO

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