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Cancer-associated fibroblasts downregulate type I interferon receptor to stimulate intratumoral stromagenesis
Journal article   Peer reviewed

Cancer-associated fibroblasts downregulate type I interferon receptor to stimulate intratumoral stromagenesis

Christina Cho, Riddhita Mukherjee, Amy R. Peck, Yunguang Sun, Noreen McBrearty, Kanstantsin V. Katlinski, Jun Gui, Priya K. Govindaraju, Ellen Pure, Hallgeir Rui, …
Oncogene, Vol.39(38), pp.6129-6137
09/17/2020
DOI: 10.1038/s41388-020-01424-7
PMCID: PMC7502515
PMID: 32807917
url
https://www.ncbi.nlm.nih.gov/pmc/articles/7502515View
Open Access

Abstract

Activation of cancer-associated fibroblasts (CAFs) and ensuing desmoplasia play an important role in the growth and progression of solid tumors. Here we demonstrate that, within colon and pancreatic ductal adenocarcinoma tumors, efficient stromagenesis relies on downregulation of the IFNAR1 chain of the type I interferon (IFN1) receptor. Expression of the fibroblast activation protein (FAP) and accumulation of the extracellular matrix (ECM) was notably impaired in tumors grown in theIfnar1(S526A)(SA) knock-in mice, which are deficient in IFNAR1 downregulation. Primary fibroblasts from these mice exhibited elevated levels of Smad7, a negative regulator of the transforming growth factor-beta (TGF beta) pathway. Knockdown of Smad7 alleviated deficient ECM production in SA fibroblasts in response to TGF beta. Analysis of human colorectal cancers revealed an inverse correlation between IFNAR1 and FAP levels. Whereas growth of tumors in SA mice was stimulated by co-injection of wild type but not SA fibroblasts, genetic ablation of IFNAR1 in fibroblasts also accelerated tumor growth. We discuss how inactivation of IFNAR1 in CAFs acts to stimulate stromagenesis and tumor growth.
Biochemistry & Molecular Biology Cell Biology Genetics & Heredity Life Sciences & Biomedicine Oncology Science & Technology

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