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Aberrant expression and mutations of 2 other members of the family, EGFR and HER2, are key carcinogenic events in several types of tumors, and both are well\u2010 validated therapeutic targets. In this study, we show that HER3 is required to maintain the motile and invasive phenotypes of prostate (DU\u2010145) and breast (MCF\u20107) cancer cells in response to the HER3 ligand neuregulin\u20101 (NRG\u20101), epidermal growth factor (EGF) and fetal bovine serum. Although MCF\u20107 breast cancer cells appeared to require HER3 as part of an autocrine response induced by EGF and FBS, the response of DU\u2010145 prostate cancer cells to these stimuli, while requiring HER3, did not appear to involve autocrine stimulation of the receptor. DU\u2010145 cells required the expression of HER3 for efficient clonogenicity <jats:italic>in vitro<\/jats:italic> in standard growth medium and for tumorigenicity in immunodeficient mice. These observations suggest that prostate cancer cells derived from tumors that overexpress HER3 are dependent on its expression for the maintenance of major attributes of neoplastic aggressiveness, with or without cognate ligand stimulation. \u00a9 2009 UICC<\/jats:p>","DOI":"10.1002\/ijc.24651","type":"journal-article","created":{"date-parts":[[2009,6,15]],"date-time":"2009-06-15T19:09:24Z","timestamp":1245092964000},"page":"2565-2575","source":"Crossref","is-referenced-by-count":40,"title":["HER3 is required for the maintenance of neuregulin\u2010dependent and \u2010independent attributes of malignant progression in prostate cancer 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