Comparative Analysis of the Effects of 17-Beta Estradiol on Proliferation, and Apoptosis in Hepatocellular Carcinoma Hep G2 and LCL-PI 11 Cell Lines

Abstract

Background: Phytoestrogens are a group of natural compounds with estrogen-like activity and similar structure<br />to estradiol that structurally mimic the mammalian estrogen 17-β estradiol (E2). They have a biphasic effect and exert<br />pleiotropic effects which induce or inhibit estrogen action by activation/inhibition of the estrogen receptors (ERs).<br />These compounds can induce apoptosis at high concentrations. The previous finding indicated that E2 inhibited cell<br />growth and induced apoptosis in hepatocellular carcinoma (HCC) PLC/PRF/5 cell line. The aim of the present study<br />was to investigate the apoptotic and proliferative effects of E2 on hepatocellular carcinoma HepG 2 and LCL-PI 11<br />cells. Methods: The Hep G2 and LCL-PI 11 cells were cultured and treated with E2 for different time periods and then<br />MTT [3-(4, 5-dimethyl-2-thiazolyl) -2, 5-diphenyl -2H- tetrazolium bromide] assay and flow cytometry assay were<br />done to determine cell viability and cell apoptosis respectively. Results: E2 had inhibitory and apoptotic effects on Hep<br />G2 cell line, whereas it indicated a biphasic effect on LCL-PI 11 cell line. The half-maximum inhibitory concentration<br />(IC50) value was 3 μM. The inhibitory effect of E2 on Hep G2 cells was observed with all concentrations of E2 (P<br /><0.087), whereas E2 showed a biphasic effect on LCL-PI 11. This compound induced significant apoptosis in Hep G2<br />cell line at the all treatment times versus control groups, whereas, in the LCL-PI 11 cell, significant apoptotic cells were<br />observed after 72 and 96h (P <0.001). Conclusion: E2 can inhibit cell growth and induce apoptosis in hepatocellular<br />carcinoma HepG 2 and LCL-PI 11 cell lines.