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Disruption of pancreatic stellate cell myofibroblast phenotype promotes pancreatic tumour invasion.

ABSTRACT: Disruption of pancreatic stellate cell myofibroblast phenotype promotes pancreatic tumour invasion.

PROVIDER: PRJNA781214 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16965250_1.fastq.gz	Fastqsanger.gz
	SRR16965250_2.fastq.gz	Fastqsanger.gz
	SRR16965251_1.fastq.gz	Fastqsanger.gz
	SRR16965251_2.fastq.gz	Fastqsanger.gz
	SRR16965252_1.fastq.gz	Fastqsanger.gz

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Disruption of pancreatic stellate cell myofibroblast phenotype promotes pancreatic tumour invasion.

Project description:In pancreatic ductal adenocarcinoma (PDAC), differentiation of pancreatic stellate cells (PSCs) into myofibroblast-like cancer-associated fibroblasts (CAFs) promotes fibrotic, therapy-resistant tumours. Conversely, suppression of CAFs can result in aggressive metastatic tumours. Here we show that the Rho-effector kinase protein kinase N2 (PKN2) is critical for PSC myofibroblast differentiation. Loss of PKN2 was associated with reduced PSC proliferation and contractility, retention of lipid droplets and decreased a-SMA stress fibres. PKN2 loss was also associated with a myofibroblast CAF to -like inflammatory CAF switch in the PSC matrisome signature both in vitro and in vivo. In spheroid co-cultures with PDAC cells, loss of PKN2 prevented PSC invasion but, counter-intuitively, promoted invasive cancer cell outgrowth. Further, deletion of PKN2 in the pancreatic stroma induced more locally invasive, orthotopic pancreatic tumours. Finally, we demonstrated that a PKN2KO PKN2 KO matrisome signature predicts poor outcome in pancreatic and other solid human cancers. Our data indicate that suppressing PSC myofibroblast differentiation function can limit important stromal tumour suppressive mechanisms, while promoting a switch to a cancer-supporting CAF phenotype.

2021-11-19 | GSE189027 | GEO

Disruption of pancreatic stellate cell myofibroblast phenotype promotes pancreatic tumor invasion.

Project description:In pancreatic ductal adenocarcinoma (PDAC), differentiation of pancreatic stellate cells (PSCs) into myofibroblast-like cancer-associated fibroblasts (CAFs) can both promote and suppress tumor progression. Here, we show that the Rho effector protein kinase N2 (PKN2) is critical for PSC myofibroblast differentiation. Loss of PKN2 is associated with reduced PSC proliferation, contractility, and alpha-smooth muscle actin (α-SMA) stress fibers. In spheroid co-cultures with PDAC cells, loss of PKN2 prevents PSC invasion but, counter-intuitively, promotes invasive cancer cell outgrowth. PKN2 deletion induces a myofibroblast to inflammatory CAF switch in the PSC matrisome signature both in vitro and in vivo. Further, deletion of PKN2 in the pancreatic stroma induces more locally invasive, orthotopic pancreatic tumors. Finally, we demonstrate that a PKN2KO matrisome signature predicts poor outcome in pancreatic and other solid human cancers. Our data indicate that suppressing PSC myofibroblast function can limit important stromal tumor-suppressive mechanisms, while promoting a switch to a cancer-supporting CAF phenotype.

| S-EPMC8810397 | biostudies-literature

Transcriptional changes in response to TGFB in human pancreatic stellate cells with knockdown of PIN1

Project description:Pancreatic stellate cells can be activated to a myofibroblast phenotype in response to TGFB treatment. The goal of this study was to determine how loss of PIN1 affects stellate cell state at baseline and in response to TGFB treatment.

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Transcriptional changes in response to TGFB in human pancreatic stellate cells with inhibition of PIN1

Project description:Pancreatic stellate cells can be activated to a myofibroblast phenotype in response to TGFB treatment. The goal of this study was to determine how inhibition of PIN1 affects stellate cell state at baseline and in response to TGFB treatment.

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Chromatin accessibility changes in response to TGFB in human pancreatic stellate cells with knockdown of PIN1

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Extracellular matrix targeted mRNA profiles of PKN2 KO/WT mouse pancreatic stellate cell lines (PSCs) treated with TGF-b or vehicle control

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Expression data from pancreatic stellate cells

Project description:tumor-stroma crosstalk drives pancreatic carcinogenesis we used time-resolved genome-wide transcriptional profiling to analyse changes caused by co-exposure of pancreatic tumor and stellate cells Primary pancreatic Stellate cells (PSC) were treated with a cumulative supernatant of pancreatic tumor cell lines (n=8) and harvested at 1-7, and 24 hours post exposure for RNA extraction and hybridization on Affymetrix microarrays. The 8 tumor cell lines are pancreatic ductal adenocarcinoma lines: AsPC1, BxPC3, Capan1, Colo357, MiaPaca2, Panc1, Su8686, and T3M4

2013-08-09 | E-GEOD-49583 | biostudies-arrayexpress

Expression data from pancreatic stellate cells

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Circulating pancreatic stellate cells: a new window into pancreatic cancer metastasis

Project description:This study aims to identify and characterise circulating pancreatic stellate cells in an orthotopic mouse model of pancreatic cancer using single cell RNA sequencing.

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Genome wide analysis of pancreatic cancer cell gene expresison exposed to stromal pancreatic stellate cells in 3D gel matrix

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2013-03-23 | E-GEOD-36775 | biostudies-arrayexpress

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