Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Anoikis resistance drives transcriptional plasticity in pancreatic cancer

ABSTRACT: Anoikis resistance drives transcriptional plasticity in pancreatic cancer

PROVIDER: PRJNA836487 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR19142800.fastq.gz	Fastqsanger.gz
	SRR19142718.fastq.gz	Fastqsanger.gz
	SRR19142719.fastq.gz	Fastqsanger.gz
	SRR19142751.fastq.gz	Fastqsanger.gz
	SRR19142752.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 74

Similar Datasets

Acquired anoikis resistance mediates enhancer-driven subtype plasticity in pancreatic cancer [ChIP-Seq]

Project description:Acquired anoikis resistance mediates enhancer-driven subtype plasticity in pancreatic cancer [ChIP-Seq]

| PRJNA836436 | ENA

Acquired anoikis resistance mediates enhancer-driven subtype plasticity in pancreatic cancer [ATAC-Seq]

Project description:Acquired anoikis resistance mediates enhancer-driven subtype plasticity in pancreatic cancer [ATAC-Seq]

| PRJNA836437 | ENA

Acquired anoikis resistance mediates enhancer-driven subtype plasticity in pancreatic cancer [RNA-seq]

Project description:Acquired anoikis resistance mediates enhancer-driven subtype plasticity in pancreatic cancer [RNA-seq]

| PRJNA836499 | ENA

Adaptive anoikis resistance promotes ovarian cancer metastasis

Project description:Anoikis resistance or evasion of cell death triggered by cell detachment is a hallmark of cancer that is concurrent with cell survival and metastasis. Phenotypes of anoikis resistant cancer cells have been extensively investigated, however, how exposure to suspension stress may lead to acquisition of a anoikis resistance phenotype has not been previously described in detail. Here we show using a spectrum of ovarian cancer cells, that cycles of suspension stress followed by attached growth, leads to adaptation and acquisition of resistance to cell death in suspension . Comparing the stepwise transcriptomic changes as cells acquire resistance, we find strong transcriptional reprogramming in the population with a majority of differentially expressed genes being downregulated during progressive acquisition of anoikis resistance. Adapted anoikis resistant cells display an enhanced dependency on oxidative phosphorylation and are capable of evasion from T cell-mediated immune surveillance. We find that such acquired anoikis resistance is not genetic. However, transcriptional reprogramming is essential to this process as acquisition of such adaptive anoikis resistance invitro and invivo are both exquisitely sensitive to specific inhibition of transcriptional reprogramming. Our data demonstrate that recovery from the verge of anoikis leads to adaptation that promotes metastasis in ovarian cancer, but can be therapeutically prevented by specific inhibitors to transcriptional reprogramming.

2024-12-01 | GSE241546 | GEO

Acquired anoikis resistance mediates enhancer-driven subtype plasticity in pancreatic cancer [ChIP-Seq]

Project description:Genetic aberrations, including mutations or deletions in KRAS, TP53, SMAD4, and CDKN2A, are common causes of pancreatic ductal adenocarcinoma (PDA). Recent large-scale transcriptomic studies demonstrated that heterogeneous gene expressions played an essential role in determining molecular subtypes of PDA, although it remains unclear what the biological cues and consequences of distinct transcriptional programs are. Here, we describe an anoikis-induction-based experimental model that enforces the transition toward a squamous subtype of PDA cells. Characteristics of the squamous subtype, represented by aggressive behaviors, are faithfully recapitulated in vitro and in vivo, demonstrating the physiological relevance of this model. Integrated analysis of epigenome and transcriptome reveals that squamous subtype PDA cells acquire pro-angiogenic enhancer activity of which is sustained by the transcription factor TEAD2. Genetic and pharmacological inhibition of TEAD2 of these tumor cells impairs their pro-angiogenic phenotypes in vitro and cancer progression in vivo. Furthermore, we found that CD109 is a critical TEAD2 target that retains activated JAK-STAT signaling. Together, our findings implicate a TEAD2-CD109-JAK/STAT axis as a potential therapeutic vulnerability concealed in the squamous subtype-associated epigenome of pancreatic cancer cells.

2023-04-04 | GSE202527 | GEO

Acquired anoikis resistance mediates enhancer-driven subtype plasticity in pancreatic cancer [ATAC-Seq]

2023-04-04 | GSE202526 | GEO

Acquired anoikis resistance mediates enhancer-driven subtype plasticity in pancreatic cancer [RNA-seq]

2023-04-04 | GSE202532 | GEO

Anoikis resistance drives transcriptional plasticity in pancreatic cancer

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

2023-04-04 | GSE202534 | GEO

Gene expression signatures in anoikis-resistance of human prostate PC-3 cells

Project description:To investigate potential molecular targets that regulate metastasis and metabolism in anoikis-resistance of prostate cancer cells, we have establised anoikis-resistant prostate PC-3 cells with ultra-low attachment 6-well plates (Corning) and employed whole genome microarray expression profiling as a discovery platform to identify differentially expressed genes between anoikis-resistant PC-3 cells and corresponding parental cells.

2020-06-26 | GSE100629 | GEO

Adaptive anoikis resistance promotes ovarian cancer metastasis

Project description:Adaptive anoikis resistance promotes ovarian cancer metastasis

| PRJNA1008671 | ENA