Abstract 1309: ERβ1 induces apoptosis in lung cancer cells by regulating growth factor signaling.

Abstract

Abstract Estrogens have recently been associated with the clinical outcome of patients with non-small cell lung cancer (NSCLC). The wild-type estrogen receptor β (ERβ1) one of the mediators of the estrogen signaling in cells is expressed in lung cancer. However, the role of ERβ1 in NSCLC cell growth has not been fully elucidated. Here we show that induction of ERβ1 expression inhibited cell growth in H1299 and A549 NSCLC cells. Treatment of these cells with the ERβ agonists 17β-estradiol or 3β-Adiol further decreased cell proliferation and induced apoptosis. ERβ1 was found to induce apoptosis through stimulation of the intrinsic apoptotic pathway that involves upregulation of the proapoptotic protein Bim. Inactivation of the extracellular-signal-regulated kinases ERK1/2 was found to be involved in the ERβ1-mediated induction of apoptosis since treatment with EGF that activates ERK1/2 abolished the ability of ERβ1 to sustain the apoptotic phenotype. These results suggest that, by regulating NSCLC cell growth, ERβ1 could be an important factor in biology of lung cancer and a potentially useful component in the clinical management of the disease. Citation Format: Christoforos Thomas, Fotis Nikolos, Gayani Rajapaksa, Igor Bado, Jan-Ake Gustafsson. ERβ1 induces apoptosis in lung cancer cells by regulating growth factor signaling. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1309. doi:10.1158/1538-7445.AM2013-1309