Human breast carcinoma desmoplasia is PDGF initiated View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2000-09

AUTHORS

Zhi-Ming Shao, Mai Nguyen, Sanford H Barsky

ABSTRACT

The desmoplastic response to human breast carcinoma is a host myofibroblast-mediated collagenous response exhibiting synergistic effects on tumor progression. Although many paracrine interactions between breast carcinoma cells and myofibroblasts have been characterized, the event(s) which initiate desmoplasia have remained undefined. Our studies utilized c-rasH transfected MCF-7 cells which overexpress ras p2l and which are weakly tumorigenic in ovariectomized nude mice. The xenografts are desmoplastic and comprised of 30% myofibroblasts and 60 mg/g of interstitial collagen. In situ hybridization studies of these xenografts reveal a stromal gene expression pattern (stromelysin-3, IGF-II and TIMP-1) identical to that observed in human tumor desmoplasia. 17-beta estradiol increases c-rasH MCF-7 growth but abolishes desmoplasia. c-rasH MCF-7 in vitro constitutively produce myofibroblast mitogenic activity which competes with PDGF in a receptor binding assay. This myofibroblast mitogenic activity is unaltered by 17-beta estradiol/tamoxifen pretreatment in vitro. Transfection of c-rasH MCF-7 with a PDGF-A dominant negative mutant, 1308, produced by site-directed mutagenesis (serine-->cysteine129) reduces both homo- and heterodimer secretion of PDGF by as much as 90% but does not interfere with the secretion of other growth factors. Clones with low PDGF, though tumorigenic, are non-desmoplastic. Our results suggest that breast carcinoma-secreted PDGF is the major initiator of tumor desmoplasia. More... »

PAGES

4337

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.onc.1203785

DOI

http://dx.doi.org/10.1038/sj.onc.1203785

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1014485677

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/10980609


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