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Tumour Cell Heterogeneity Instructs Fibroblast Diversity and Reciprocal Signalling [dataset 2]

ABSTRACT: Tumour Cell Heterogeneity Instructs Fibroblast Diversity and Reciprocal Signalling [dataset 2]

PROVIDER: PRJNA558891 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9908940_1.fastq.gz	Fastqsanger.gz
	SRR9908940_2.fastq.gz	Fastqsanger.gz
	SRR9908950_1.fastq.gz	Fastqsanger.gz
	SRR9908950_2.fastq.gz	Fastqsanger.gz
	SRR9908960_1.fastq.gz	Fastqsanger.gz

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Tumour Cell Heterogeneity Instructs Fibroblast Diversity and Reciprocal Signalling

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Tumour Cell Heterogeneity Instructs Fibroblast Diversity and Reciprocal Signalling [dataset 2]

Project description:We investigated changes to murine pancreatic fibroblast gene expression in response to co-culture with 8 murine pancreatic tumour cell sub-populations. Tumours are complex ecosystems where phenotypically diverse tumour cells are embedded in a heterocellular environment. Using an in vitro model of intra-tumoral heterogeneity, we show that clonal tumour cell populations establish distinct interactions with stromal fibroblasts to expand phenotypic diversity across tumour and stromal cell populations. Heterocellular interactions drive differential engagement of tumour cell reciprocal signalling pathways, resulting in normalisation of cell-autonomous differences in MAPK signalling but diversification of AKT signalling. Consequently, tumour cell clones display differential cell-autonomous and non-cell autonomous dependencies. These results demonstrate that tumour-stroma interactions amplify tumour cell autonomous diversity and that our existing perspective on tumour cell heterogeneity underestimates functional diversity.

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Tumour Cell Heterogeneity Instructs Fibroblast Diversity and Reciprocal Signalling

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Heterocellular OSM-OSMR signalling drives pancreatic cancer growth and metastasis through functional fibroblast reprogramming

Project description:Pancreatic ductal adenocarcinoma (PDA) is a lethal malignancy characterised by a pathological fibroinflammatory microenvironment. Dichotomous tumour-promoting and -restrictive roles have been ascribed to the tumour microenvironment, however the effects of individual stromal subsets remains incompletely characterised. Here, we describe how heterocellular OSM-OSMR signalling instructs fibroblast reprogramming, tumour growth and metastasis. Macrophage-secreted OSM stimulates inflammatory gene expression in cancer-associated fibroblasts (CAFs), which in turn induce a pro-tumorigenic environment and engage tumour cell survival and migratory signalling pathways. Tumour cells implanted in Osm-deficient (Osm-/-) mice display an epithelial-dominated morphology, reduced tumour growth and did not metastasise. Moreover, the tumour microenvironment of Osm-/- animals exhibit increased abundance of αSMApos myofibroblasts and a shift in myeloid and T cell phenotypes, consistent with a more immunogenic environment. Taken together, these data demonstrate how OSM-OSMR signalling coordinates heterocellular interactions to drive a pro-tumorigenic environment in PDA.

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