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RNA seq on primary pancreatic cancer cells growing on collagen 1 homotrimers and heterotrimers

ABSTRACT: RNA seq on primary pancreatic cancer cells growing on collagen 1 homotrimers and heterotrimers

PROVIDER: PRJNA544331 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9110410_1.fastq.gz	Fastqsanger.gz
	SRR9110410_2.fastq.gz	Fastqsanger.gz
	SRR9110420_1.fastq.gz	Fastqsanger.gz
	SRR9110420_2.fastq.gz	Fastqsanger.gz
	SRR9110430_1.fastq.gz	Fastqsanger.gz

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RNA seq on primary pancreatic cancer cells growing on collagen 1 homotrimers and heterotrimers

Project description:RNA seq on primary pancreatic cancer (KPPC;Col1pdxKO cancer-collagen1 knockout) cells growing on collagen 1 homotrimers and heterotrimers. In this study, we identify that pancreatic cancer cells produce a unique Collagen1 homotrimer variant, in contrast to the Collagen1 heterotrimer produced by normal cells (such as fibroblasts). The variant forms of Collagen1 (homotrimer and heterotrimer) have distinct effects on cancer cell behaviors. We culture the pancreatic cancer cells on purified Collagen1 homotrimer and heterotrimer (as well as vehicle control) and examine the global changes of gene expression profile in cancer cells by variant Collagen1 subtypes.

2022-05-21 | GSE131666 | GEO

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The GLP-1R agonist semaglutide reshapes pancreatic cancer associated fibroblasts reducing collagen hydroxyprolination and favoring immune infiltration.

Project description:Metabolic syndrome represents a risk factor of pancreatic ductal adenocarcinoma (PDAC), the gastrointestinal cancer with the lowest survival rate and therapeutic outcome. PDAC results bidirectional interconnected with metabolic alteration, which favors its onset and occurs during early phases of its development. Pancreatic neoplastic lesions evolve within a highly dense desmoplastic stroma, characterized by abundant extracellular matrix deposition consequence of a prominent cancer associated fibroblast (CAF) activation. Here, the complex association between dysmetabolism and PDAC has been analyzed with a specific focus on CAFs to unveil novel targets exploitable for diagnostic and therapeutic purposes. Methods: PDAC development upon dysmetabolic conditions was investigated in: 1) wild type immunocompetent syngeneic mice by orthotopic transplantation of PanIN-bearing Pdx1-Cre; Kras+/LSL-G12D; Trp53+/LSL-R172H organoids (KPC mice) fed with high fat diet to recapitulate dysmetabolism-dependent alterations; and 2) primary pancreatic CAFs isolated from chemotherapy naïve PDAC patients with or without an history of metabolic syndrome. Results: The dysmetabolic-associated higher PDAC aggressiveness was paralleled by an enrichment of collagen fibrils due to an increased function of the prolyl 4-hydroxylase subunit alpha 1 (P4HA1). Upon dysmetabolic conditions, P4HA1 boosts collagen hydroxy-prolination, intensifying collagen contraction strength and thus preventing CD3 positive lymphocyte PDAC infiltration. Interestingly, semaglutide, an incretin agonist with anti-diabetic and anti-obesity properties, is able to prevent the higher stromal deposition of PDAC observed in dysmetabolic conditions, preventing CAF contraction, allowing immune infiltration and reducing tumor development. Conclusion: These results shed light on novel therapeutic options for PDAC patients affected by metabolic syndrome aimed at pancreatic cancer stroma reshape

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RNA seq on two primary pancreatic cancer cell lines (cancer-collagen1 knockout cell line and control pancreatic cancer cell line)

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Project description:Despite the well described role of non-cellular components of the tumor microenvironment (TME) in regulating tumor growth, the molecular events dictating expression and biological functions of key components of the TME remain elusive. Here, using pancreatic cancer (PC) models, we describe a novel mechanism through which the zinc finger transcription factor GLI2 in cancer associated fibroblasts (CAFs) induces expression of COL1A1, which is a major component of Collagen I and the most abundant collagen variant in the tumor milieu. Bulk and single nuclei RNA-seq showed that GLI2 expression in CAF strongly correlates with COL1A1 levels, fibrosis, and CAF activation. ChIP-qPCR and expression studies of the PC matrisome identified COL1A1 as the direct target of GLI2 in CAFs. We also provide evidence that GLI2 is an effector that mediates COL1A1 induction by transforming growth factor β1 (TGFβ1). RNA-seq analysis of PC cells treated with Collagen I revealed enrichment of chemotherapeutic gene expression profiles, which includes irinotecan resistance signature. Viability studies confirmed that Collagen I promotes irinotecan resistance in PC cells. Altogether, our results uncover a novel role for the TGFβ1-GLI2 axis within CAFs to modulate Collagen I expression and promote chemoresistance in PC cells. Our findings increase our understanding of the complex molecular network operating in the TME.

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