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G Protein Estrogen Receptor (GPR30) Regulates hERG (Kv11.1) Channel Activity

Tuesday, 27 September 2011 at 17:15

Add to Calendar ▼2011-09-27 17:15:002011-09-27 18:15:00Europe/LondonG Protein Estrogen Receptor (GPR30) Regulates hERG (Kv11.1) Channel ActivityIon Channel Targets in San FranciscoSan FranciscoSELECTBIOenquiries@selectbiosciences.com

Research in cancer biology has revealed that the hERG1 gene encoding Kv11.1 potassium ion channel is robustly expressed in breast cancers but not in adjacent non-neoplastic tissue. Blocking Kv11.1 current inhibits proliferation of human cancer cells, suggesting that this channel plays a significant role in the biology of cancerous tissue. Breast cancer cells that do not express estrogen receptors (ERneg) manifest an estrogen-dependent aggressive course of disease and have high rates of metastasis compared to other histological types. Although treatments that target the ER have recently proven very promising ERneg cancers do not respond to ER-targeted therapies, as they lack canonical a/b-estrogen receptors. Interestingly, recent studies have demonstrated that estrogen effects on proliferation of ERneg breast cancer cells can be mediated by the novel membrane bound estrogen receptor, GPER (GPR30). However, very little is known about the biochemical signaling cascade activated by estrogen via GPER. Here we show that: Kv11.1 ion channel activity is modulated by an estrogen-activated signaling cascade via the newly characterized membrane bound estrogen receptor GPER in ERneg breast cancer cells.