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Expression of estrogen receptor alpha increases leptin‐induced STAT3 activity in breast cancer cells by Nadine A. Binai; Annette Damert; Gert Carra; Stephan Steckelbroeck; Johannes Löwer; Roswitha Löwer; Silja Wessler is a Medicine article available to read on EtoBox.
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## Abstract Adipositas correlates with an enhanced risk of developing malignant diseases such as breast cancer, endometrial tumor or prostate carcinoma, but the molecular basis for this is not well understood. Potential mechanisms include increased bioavailability of adipocytokines (__e.g.__ leptin) and steroid hormones. Here, we investigated cross‐talk between ERα (estrogen receptor alpha) and leptin‐induced activation of signal transducer and activator of transcription 3 (STAT3), a transactivator of important oncogenes. Upon leptin binding to its receptor Ob‐RL (obesity receptor), STAT3 tyrosine phosphorylation and transactivation activity were enhanced by simultaneously expressing ERα. Downregulation of ERα using small interfering RNA abolished leptin‐induced STAT3 phosphorylation. Interestingly, leptin‐mediated STAT3 activation was unaffected by co‐stimulation with the ERα ligands estradiol (E2) or estrogen antagonists ICI182,780 and tamoxifen, implying that enhancement of leptin‐mediated STAT3 activity is independent of ERα ligands. We also detected ERα binding to STAT3 and JAK2 (Janus kinase 2), resulting in enhanced JAK2 activity upstream of STAT3 in response to leptin that
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- Author
- Nadine A. Binai; Annette Damert; Gert Carra; Stephan Steckelbroeck; Johannes Löwer; Roswitha Löwer; Silja Wessler
- Publisher
- John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley; Research Square; Test accounts (ISSN 0020-7136)
- Published
- 2010
- Language
- EN
- Field
- Medicine (Health Sciences)