Int J Biol Sci 2019; 15(5):942-952. doi:10.7150/ijbs.30930

Research Paper

Estrogen Receptor Beta (ERβ) Mediated-CyclinD1 Degradation via Autophagy Plays an Anti-Proliferation Role in Colon Cells

Yong Wei1, Can Huang2, Haoyu Wu1, Jian Huang1✉

1. Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, Hubei, P.R China
2. Wuhan Agricultural Inspection Center, Hubei, P.R China

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Citation:
Wei Y, Huang C, Wu H, Huang J. Estrogen Receptor Beta (ERβ) Mediated-CyclinD1 Degradation via Autophagy Plays an Anti-Proliferation Role in Colon Cells. Int J Biol Sci 2019; 15(5):942-952. doi:10.7150/ijbs.30930. Available from http://www.ijbs.com/v15p0942.htm

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Abstract

Dysfunction of autophagic degradation machinery causes tumorigenesis, including colorectal cancer (CRC). Overexpression of CyclinD1 in CRC has been reported. Recent evidence also suggests that ERβ deficiency is related to the pathogenesis of CRC. Very little is known, however, about the detailed molecular mechanisms underlying the relationship among ERβ, autophagy, and CyclinD1 in CRC. Here, results showed that ERβ played an anti-proliferation role in HCT116 through impairing cell cycle but not apoptosis. Additionally, CyclinD1 accumulation was increased in response to chloroquine (CQ) or in MEF Atg7 knockout cells. Further, ERβ could inhibit the mammalian target of rapamycin (mTOR) or activate Bcl-2/adenovirus E1B 19-kDa-interacting protein 3 (BNIP3) to promote autophagy in HCT116. In summary, these results indicate that ERβ-mediated CyclinD1 degradation can inhibit colon cancer cell growth via autophagy.

Keywords: ERβ, autophagy, colorectal cancer, mTOR, BNIP3, CyclinD1