Sanaei Masumeh, Kavoosi Fraidoon, Dehghani Faeze
Research Center for Non- Communicable Diseases, Jahrom University of Medical Sciences, Jahrom, Iran. Email:
Asian Pac J Cancer Prev. 2018 Sep 26;19(9):2637-2641. doi: 10.22034/APJCP.2018.19.9.2637.
Background: Phytoestrogens are a group of natural compounds with estrogen-like activity and similar structure to estradiol that structurally mimic the mammalian estrogen 17-β estradiol (E2). They have a biphasic effect and exert pleiotropic effects which induce or inhibit estrogen action by activation/inhibition of the estrogen receptors (ERs). These compounds can induce apoptosis at high concentrations. The previous finding indicated that E2 inhibited cell growth and induced apoptosis in hepatocellular carcinoma (HCC) PLC/PRF/5 cell line. The aim of the present study was to investigate the apoptotic and proliferative effects of E2 on hepatocellular carcinoma HepG 2 and LCL-PI 11 cells. Methods: The Hep G2 and LCL-PI 11 cells were cultured and treated with E2 for different time periods and then MTT [3-(4, 5-dimethyl-2-thiazolyl) -2, 5-diphenyl -2H- tetrazolium bromide] assay and flow cytometry assay were done to determine cell viability and cell apoptosis respectively. Results: E2 had inhibitory and apoptotic effects on Hep G2 cell line, whereas it indicated a biphasic effect on LCL-PI 11 cell line. The half-maximum inhibitory concentration (IC50) value was 3 μM. The inhibitory effect of E2 on Hep G2 cells was observed with all concentrations of E2 (P <0.087), whereas E2 showed a biphasic effect on LCL-PI 11. This compound induced significant apoptosis in Hep G2 cell line at the all treatment times versus control groups, whereas, in the LCL-PI 11 cell, significant apoptotic cells were observed after 72 and 96h (P <0.001). Conclusion: E2 can inhibit cell growth and induce apoptosis in hepatocellular carcinoma HepG 2 and LCL-PI 11 cell lines.
植物雌激素是一类具有雌激素样活性且结构与雌二醇相似的天然化合物，在结构上模拟哺乳动物雌激素17-β雌二醇（E2）。它们具有双相效应并发挥多效性作用，通过激活/抑制雌激素受体（ERs）来诱导或抑制雌激素作用。这些化合物在高浓度时可诱导细胞凋亡。先前的研究发现表明，E2可抑制肝癌（HCC）PLC/PRF/5细胞系的细胞生长并诱导其凋亡。本研究的目的是探讨E2对肝癌HepG 2和LCL-PI 11细胞的凋亡和增殖作用。方法：培养Hep G2和LCL-PI 11细胞，并用E2处理不同时间段，然后分别进行MTT [3-(4, 5-二甲基-2-噻唑基)-2, 5-二苯基-2H-溴化四唑] 法和流式细胞术检测，以分别测定细胞活力和细胞凋亡情况。结果：E2对Hep G2细胞系具有抑制和凋亡作用，而对LCL-PI 11细胞系表现出双相效应。半数最大抑制浓度（IC50）值为3 μM。所有浓度的E2均对Hep G2细胞有抑制作用（P <0.087），而E2对LCL-PI 11细胞表现出双相效应。与对照组相比，该化合物在所有处理时间均能诱导Hep G2细胞系发生显著凋亡，而在LCL-PI 11细胞中，在72小时和96小时后观察到显著的凋亡细胞（P <0.001）。结论：E2可抑制肝癌HepG 2和LCL-PI 11细胞系的细胞生长并诱导其凋亡。
