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Effect of depletion of sin-lncRNA in senescent IMR90 fibroblasts

ABSTRACT: Effect of depletion of sin-lncRNA in senescent IMR90 fibroblasts

PROVIDER: PRJNA1009000 | ENA |

REPOSITORIES: ENA

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Effect of depletion of sin-lncRNA in senescent IMR90 fibroblasts

Project description:Despite the classical view of senescence as passive growth arrest, it is an active process with profound implications for cellular homeostasis. Indeed, senescent cells remain metabolically active to be able to cope with the energetic demand of the senescence program, although the precise mechanisms underlying this metabolic reprogramming are just beginning to emerge. Here we have identified sin-lncRNA, a previously uncharacterized lncRNA, highly specific of senescent cells, and transcriptionally induced by the master regulator of senescence C/EBPβ. While being strongly activated in senescence, sin-lncRNA knockdown reinforces the senescence program by altering oxidative phosphorylation and impairing mitochondrial function. Sin-lncRNA interacts with the TCA enzyme dihydrolipoamide S-succinyltransferase (DLST) to facilitate its proper function. sin-lncRNA depletion increases DLST nuclear translocation, favoring a metabolic shift from oxidative phosphorylation to a glycolytic phenotype. Moreover, while sin-lncRNA expression remains low in highly proliferative cancer cells, it is strongly induced upon cisplatin-induced senescence. Knockdown of sin-lncRNA in ovarian cancer cells results in deficient oxygen consumption and increased extracellular acidification, sensitizing the cells to cisplatin treatment. Altogether, these results indicate that sin-lncRNA is specifically induced in cellular senescence to maintain metabolic homeostasis. Our findings reveal a new regulatory mechanism in which lncRNA contributes to the adaptive metabolic changes in senescent cells, unveiling the existence of an RNA-dependent metabolic network specific to senescent cells.

2025-04-29 | GSE241620 | GEO

sin-lncRNA interactors in senescent fibroblasts MS

Project description:sin-lncRNA is a noncoding RNA molecule with a role in cellular senescence. In vitro RNA pulldown of biotynilated sin-lncRNA was performed to identify sin-lncRNA specific protein partners

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Transcription profiling of human IMR90 cells after RNAi suppression of RB, p107 or p130 using in growing, quiescent or ras-induced senescent IMR90 cells

Project description:The action of RB as a tumor suppressor has been difficult to define, in part, due to the redundancy of the related proteins p107 and p130. By coupling advanced RNAi technology to suppress RB, p107 or p130 with a genome wide analysis of gene expression in growing, quiescent or ras-senescent cells, we identified a unique and specific activity of RB in repressing DNA replication as cells exit the cell cycle into senescence, a tumor suppressive program. Experiment Overall Design: Expression profiles of IMR90 cells before and after RNAi-mediated supppression of RB, p107 or p130 in growing, quiescent or ras-induced senescent conditions. RNA was extracted from growing, low serum (0.1% FBS), confluent, or ras-senescent cells.

2010-01-23 | E-GEOD-19864 | biostudies-arrayexpress

Deep sequencing of human fibroblastic cell line IMR90, either proliferating or senescent, with or without TSA treatment.

Project description:Gene expression changes were compared in proliferating and senescent human IMR90 cells, with or without TSA treatment. Method: RNA was extracted, in triplicate, then sequenced with an Illumina NextSeq 500 sequencer. Sequence reads passing the quality control filters were aligned using Tophat2 and then analysed with Cufflinks.

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Effect of SMARCA4 knockdown on senescent IMR90 ER:RAS cells

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Phosphorylation level of SIRT1 in proliferating and senescent IMR90 cells

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Expression data from either growing IMR90 human fibroblasts or senescent IMR90 cells with Ras expression and indicated hairpins

Project description:Oncogene-induced senescence is an anti-proliferative stress response program that acts as a fail-safe mechanism to limit oncogenic transformation and is regulated by the retinoblastoma protein (RB) and p53 tumor suppressor pathways. We identify the atypical E2F family member E2F7 as the only E2F transcription factor potently upregulated during oncogene-induced senescence, a setting where it acts in response to p53 as a direct transcriptional target. Once induced, E2F7 binds and represses a series of E2F target genes and cooperates with RB to efficiently promote cell cycle arrest and limit oncogenic transformation. Disruption of RB triggers a further increase in E2F7, which induces a second cell cycle checkpoint that prevents unconstrained cell division despite aberrant DNA replication. Mechanistically, E2F7 compensates for the loss of RB in repressing mitotic E2F target genes. To understand the contribution of different genes, especially E2F7 to the expression profile of senescent cells, we infected human IMR90 cells with Ras and different hairpins. The infected population was selected using first with 2 ug/ml puromycin (Sigma) for 2 days, then 100 ug/ml hygromycin B (Roche) for 3 days. RNA was isolated 7 days after the puromycin selection and hybridized to Affymetrix microarrays. We tried to understand the effect of E2F7 in the transcription profile of senescent cells.

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