Abstract 3931: Progesterone and estrogen affect the expression and secretion of heparin binding epidermal growth factor like growth factor (HB-EGF) in RL95-2 cells, an endometrial cancer cell line

Abstract

Abstract Endometrial cancer is one of the most common gynecological cancers. Heparin Binding Growth Factor-like Growth Factor exerts acute effects on cancer cells; in that it induces and promotes proliferation and hence the pathogenesis and progression of endometrial cancer. Steroid hormones directly or indirectly affect the expression of HB-EGF and may thus play a role in the malignant transformation of endometrial cells. The aim of this project is therefore to evaluate the effects of progesterone (P4) and estrogen (E2) treatments on the expression and secretion of HB-EGF in endometrial cancer cells. We hypothesized that P4 will reduce HB-EGF expression and secretion while E2 will increase its expression and secretion. To test our hypothesis, an endometrial cell line, RL95-2, was treated for four days asfollows: (1) 10−8M E2, (2)10−6M P4, (3) 10−8M E2 + 10−6M P4 (4) 10−8M E2 in two days followed by 10−6M P4 and (5) Control. Immunocytochemistry (ICC), ELISA and western blot analysis were performed to evaluate the secretion and expression of HB-EGF in RL95-2 cells. Western blot analysis and ICC showed a consistently enhanced expression of HB-EGF in cells treated with E2 and in cells treated with E2 followed by P4 relative to the control groups. Alternatively, cells treated with P4 showed a down-regulation of HB-EGF expression relative to the control group. ELISA analysis showed high secretion of HB-EGF in cells treated with E2 and cells treated with E2 followed by P4 relative to the control groups. The secretion of HB-EGF was lower in cells treated with P4 alone compared to the control. In sum, there is an acute effect of E2 and P4 on the expression and secretion of HB-EGF and thus consequently may affect endometrial cancer cell proliferation. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3931. doi:1538-7445.AM2012-3931