ERβ up-regulation was involved in silibinin-induced growth inhibition of human breast cancer MCF-7 cells

Archives of Biochemistry and Biophysics
Nan ZhengTakashi Ikejima

Abstract

We previously reported that silibinin induced a loss of cell viability in breast cancer (MCF-7) cells by ERα down-regulation. But whether this cytotoxicity depends on another estrogen receptor, ERβ, has yet to be elucidated. Therefore, we sought to explore the effects of ERβ modulation on cell viability by using an ERβ-selective agonist (Diarylprepionitrile, DPN) and an antagonist (PHTPP). Our data demonstrated that ERβ served as a growth suppressor in MCF-7 cells, and the incubation of silibinin, elevated ERβ expression, resulting in the tumor growth inhibition. The cytotoxic effect of silibinin was diminished by PHTPP and enhanced by DPN. Silencing of ERβ by siRNA confirmed these results. Apoptotic cascades, including the sequential activation of caspase-9 and -6, and finally the cleavage of caspase substrates, PARP and ICAD, caused by treatment with silibinin, were all repressed by PHTPP pre-treatment but exacerbated by DPN. Unlike ERα, ERβ did not involve autophagic process in the regulation, since neither autophagic inhibitor (3-MA) nor the inducer (rapamycin) affected the cell survival rates regardless ERβ activity. Taken together, silibinin induced apoptosis through mitochondrial pathway by up-regulating ERβ pathways in ...Continue Reading

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Citations

Jul 1, 2016·Expert Review of Clinical Pharmacology·Xing-Xing ZhuQiang He
Sep 19, 2020·Biomarker Research·Yujing Zhou, Xingdang Liu
Feb 10, 2021·Journal of Photochemistry and Photobiology. B, Biology·Weiwei LiuTakashi Ikejima
Dec 21, 2019·Anti-cancer Agents in Medicinal Chemistry·Agata BiniendaElzbieta Pluciennik
Mar 24, 2018·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Jing YangTakashi Ikejima

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