Loss of TGF-β type II receptor in fibroblasts promotes mammary carcinoma growth and invasion through upregulation of TGF-α-, MSP- and ... View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2005-07

AUTHORS

Nikki Cheng, Neil A Bhowmick, Anna Chytil, Agnieszka E Gorksa, Kimberly A Brown, Rebecca Muraoka, Carlos L Arteaga, Eric G Neilson, Simon W Hayward, Harold L Moses

ABSTRACT

Stromal fibroblasts regulate epithelial cell behavior through direct and indirect cell-cell interactions. To clarify the role of TGF-beta signaling in stromal fibroblasts during mammary development and tumorigenesis, we conditionally knocked out the TGF-beta type II receptor gene in mouse mammary fibroblasts (Tgfbr2(fspKO)). Tgfbr2(fspKO) mice exhibit defective mammary ductal development, characterized in part by increased ductal epithelial cell turnover associated with an increase in stromal fibroblast abundance. Tgfbr2(fspKO) mammary fibroblasts transplanted with mammary carcinoma cells promote growth and invasion, which is associated with increased activating phosphorylation of the receptors: erbB1, erbB2, RON, and c-Met. Furthermore, the increased receptor phosphorylation correlates with increased secretion of the cognate ligands by Tgfbr2(fspKO) fibroblasts. Treatment of tumor cells with fibroblast-conditioned medium leads to increased tumor cell proliferation and motility, which are blocked by addition of pharmacologic inhibitors of TGF-alpha signaling or neutralizing antibodies to macrophage-stimulating protein (MSP), HGF, or c-Met. These studies characterize a significant role for stromal TGF-beta signaling in mammary tissue homeostasis and mammary tumor progression via regulation of TGF-alpha, MSP, and HGF signaling pathways. More... »

PAGES

1208685

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1208685

DOI

http://dx.doi.org/10.1038/sj.onc.1208685

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1024019697

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/15856015


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