Genistein inhibits the proliferation of human choriocarcinoma cells via the downregulation of estrogen receptor-α phosphorylation at serine 118

Abstract

<h2>Summary</h2><h3>Background & aims</h3> Choriocarcinoma is a malignant trophoblastic tumor. The phosphorylation of estrogen receptor-α at serine 118 (p-ER-s118) decreases cancer cell proliferation. However, the effect of genistein as a modulator of p-ER-s118 and proliferation of chorioarcinoma cells remains to be understood. This study aims at determining the function of genistein on p-ER-s118 levels and human choriocarcinoma JEG-3 cell proliferation. <h3>Methods</h3> After reaching confluency, cells were divided into six groups, the control group (without methyl-piperidino-pyrazole (MPP) pre-treatment and genistein treatment); and groups with cells treated with genistein at concentrations of 0, 10, 25, 50, and 100 μM (cells were pretreated with MPP). Expression of p-ER-s118 and Ki-67 were analyzed using immunocytochemistry. <h3>Results</h3> Different doses of genistein decreased p-ER-s118 levels compared to those in the control (<i>p</i> < 0.05). JEG-3 cell proliferation was inhibited by MPP pre-treatment, concomitant with genistein treatment with a dose of 0 μM, 25 μM, 50 μM, and 100 μM compared to the proliferation of the control cells (<i>p</i> < 0.05). <h3>Conclusion</h3> Taken together, treatment with methyl-piperidino-pyrazole downregulated p-ER-s118. The addition of genistein further decreased the levels of p-ER-s118 and inhibited cell proliferation. Thus, <i>in vivo</i> studies nedd to follow this <i>in vitro</i> study to elucidate the mechanism(s) employed by genistein as an alternative therapy for choriocarcinoma.