| First Author | Proietti CJ | Year | 2009 |
| Journal | Mol Cell Biol | Volume | 29 |
| Issue | 5 | Pages | 1249-65 |
| PubMed ID | 19103753 | Mgi Jnum | J:145722 |
| Mgi Id | MGI:3835891 | Doi | 10.1128/MCB.00853-08 |
| Citation | Proietti CJ, et al. (2009) Activation of Stat3 by heregulin/ErbB-2 through the co-option of progesterone receptor signaling drives breast cancer growth. Mol Cell Biol 29(5):1249-65 |
| abstractText | 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. |
