期刊
MOLECULAR AND CELLULAR BIOLOGY
卷 29, 期 5, 页码 1249-1265出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.00853-08
关键词
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资金
- National Agency of Scientific Promotion of Argentina [IDB 1728 OC/AR PICT 25301, 0211]
- Argentina National Council of Scientific Research [PIP 5391]
- Henry Moore Institute of Argentina [CONICET 1819/03]
Cross talk between the steroid hormone receptors for estrogen and progesterone (PR) and the ErbB family of receptor tyrosine kinases appears to be a hallmark of breast cancer growth, but its underlying mechanism remains poorly explored. Here we have highlighted signal transducer and activator of transcription 3 (Stat3) as a key protein activated by heregulin (HRG), a ligand of the ErbB receptors, through co-opted, ligand-independent PR function as a signaling molecule. Stat3 activation was an absolute requirement in HRG-induced mammary tumor growth, and targeting Stat3 effectively inhibited growth of breast cancer cells with activated HRG/ErbB-2 and PR. Our findings unravel a novel potential therapeutic intervention in PR-and ErbB-2-positive breast tumors, involving the specific blockage of PR signaling activity.
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