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Escape from TGF-β-induced senescence promotes aggressive hallmarks in epithelial hepatocellular carcinoma cells

ABSTRACT: Escape from TGF-β-induced senescence promotes aggressive hallmarks in epithelial hepatocellular carcinoma cells

PROVIDER: PRJNA1085286 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28261202.fastq.gz	Fastqsanger.gz
	SRR28261203.fastq.gz	Fastqsanger.gz
	SRR28261204.fastq.gz	Fastqsanger.gz
	SRR28261205.fastq.gz	Fastqsanger.gz
	SRR28261206.fastq.gz	Fastqsanger.gz

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Escape from TGF-β-induced senescence promotes aggressive hallmarks in epithelial hepatocellular carcinoma cells

Project description:Transforming growth factor-β (TGF-β) signaling and cellular senescence are key hallmarks of hepatocellular carcinoma (HCC) pathogenesis. While provoking senescence-associated growth arrest in epithelial HCC cells, elevated TGF-β activity paradoxically correlates with aggressiveness and poor prognosis in advanced tumors. Whether the transition between these dichotomous functions involves bypassing the senescence barrier during disease progression remains unknown. Exploiting the epithelial HCC cell line Huh7, we demonstrate that chronic TGF-β exposure prompts escape from Smad3-mediated senescence, leading to the development of TGF-β resistance. The resistant state is characterized by restoration of proliferative capacity and acquisition of molecular and functional traits of mesenchymal cells, coinciding with hybrid EMT, increased invasiveness, and metastasis. Mechanistically, resistant cells exhibit defective signaling of Smad molecules, as ectopic activation of the TGF-β/Smad3 axis reinstates TGF-β sensitivity. Gene expression landscape profiling reveals both shared and distinct gene signatures associated with senescent and TGF-β resistant states. Importantly, genetic ablation and molecular studies identify GRM8 (Glutamate Metabotropic Receptor 8) as a critical modulator of the resistance phenomenon, potentially by impairing subcellular spatiotemporal dynamics of Smad activity. Our findings unveil a novel phenomenon wherein epithelial HCC cells may exploit senescence evasion as a mechanism to oppose TGF-β anti-tumor responses and progress towards more aggressive HCC phenotypes.

2025-03-17 | GSE261099 | GEO

Bilineal differentiated liver carcinoma cells generates highly aggressive escape variants

Project description:Bilineal differentiated liver carcinoma cells generates highly aggressive escape variants

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Bilineal differentiated liver carcinoma cells generates highly aggressive escape variants

Project description:Background & Aims: Combined HCC/iCCA is a rare liver tumor type. We generated a transgenic mouse model (AlfpCre+-Trp53fl/fl/Alb-HBs+ tg mouse) which developed next to HCC combined HCC/iCCA (cHCC/iCCA). We compared bilineal differentiated liver carcinoma cell lines generated from primary liver tumors of AlfpCre+-Trp53fl/fl/Alb-HBs+ tg mice and transplanted them into C57BL/6J mice to monitor there agressiveness. We compared the geneexpression profile from those primary liver carcinoma cell lines with IFNγ treatment (pCCL-IFNγ) and without treatment (pCCL) with explanted primary carcinoma cell line (pCCL-ex). Results: Here we describe that elimination of HBs+ in pCCL by HBs/(Kb/S190-197)-specific CD8 T cells describes a potential immune escape mechanism for highly aggressive cHCC/iCCA-type liver carcinomas.

2023-05-23 | GSE215059 | GEO

Pluripotent Stem Cells Escape From Senescence-Associated DNA Methylation Changes

Project description:This SuperSeries is composed of the following subset Series: GSE37065: Long-term culture associated gene expression changes in MSC [Affymetrix] GSE37066: Pluripotent Stem Cells Escape From Senescence-Associated DNA Methylation Changes [Illumina] GSE38806: Gene expression profiles of induced pluripotent mesenchymal stromal cells [Affymetrix] Refer to individual Series

2012-09-24 | E-GEOD-37067 | biostudies-arrayexpress

Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars [Expression]

Project description:Although oncogene-induced senescence (OIS) is a potent tumor-suppressor mechanism, recent studies revealed that cells can escape from OIS with features of transformed cells. However, the mechanisms that promote OIS escape remain unclear, and evidence of post-senescent cells in human cancers is missing. Here, we unravel the regulatory mechanisms underlying OIS escape using dynamic multidimensional profiling. We demonstrate a critical role for AP1 and POU2F2 transcription factors for escape from OIS and identify ‘senescence-associated chromatin scars (SACS)’ as an epigenetic memory of OIS, detectable during colorectal cancer progression. POU2F2 levels are elevated already in precancerous lesions and as cells escape from OIS, and its expression and binding activity to cis-regulatory elements are associated with decreased patient survival. Our results support a model in which POU2F2 exploits a precoded enhancer landscape to promote senescence escape and reveal POU2F2 gene signatures and SACS as valuable biomarkers with diagnostic and prognostic potential.

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Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars [ChIP-seq]

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Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars [RNA-seq]

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Escape From Oncogene-Induced Senescence is Controlled by POU2F2 and Memorized by Chromatin Scars [ATAC-seq]

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METRONOMIC TOPOTECAN CAUSES THERAPY-INDUCED TUMOR CELL SENESCENCE AND LOSS OF AGGRESSIVE PROPERTIES IN MYCN-AMPLIFIED CHILDHOOD CANCER [Affymetrix Cytoscan HD]

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Profiling of genes regulated by TGF-beta in immortalized skin keratinocyte cells(HaCaT).

Project description:TGF-beta is one of the key cytokines implicated in various disease processes including cancer. TGF-beta inhibits growth and promotes apoptosis in normal epithelial cells and in contrast, acts as a pro-tumour cytokine by promoting tumour angiogenesis, immune-escape and metastasis. The effect of TGF-beta on the regulation of gene expression is cell-type specific. In order to identify TGF-beta regulated genes in different cell-types, we followed the expression profiling approach. Keywords: cell type specific response to TGF-beta

2007-05-01 | GSE7661 | GEO

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