Fenofibrate induced PPAR alpha expression was attenuated by oestrogen receptor alpha overexpression in Hep3B cells

• DOI: 10.1002/tox.22511
• Publication Date: 2017-11-14T06:32:50Z
• Authors: Long‐Bin Jeng; Bharath Kumar Vel...; Hsi‐Hsien Hsu; Su‐Ying Wen; Chia‐Yao Shen; Chih‐Hao Lin; Yueh‐Min Lin; Ray‐Jade Chen; Wei‐Wen Kuo; Chih‐Yang Huang
• Keywords: Alpha (finance); Fenofibrate; Oestrogen receptor; CYP17A1

Abstract The physiological regulation of Oestrogen receptor α (ERα) and peroxisome proliferator‐activated alpha (PPARα) in Hepatocellular carcinoma (HCC) remains unknown. present study we first treat the cells with fenofibrate further investigated possible mechanisms 17β‐estradiol (E 2 ) and/or ERα on regulating PPARα expression. We also found higher expression tumor area than adjacent areas subsequently compared four different hepatic cancer cell lines. Hep3B were to express more other Using agonist fenofibrate, that increased proliferation efficiency by increasing cycle proteins, such as cyclin D1 PCNA, inhibiting p27 caspase 3 expressions. Next, performed transient transfections immuno‐precipitation studies using pTRE2/ERα plasmid evaluate interaction between PPARα. interacted directly negatively regulated its function. Moreover, Tet‐on over‐expressed cells, E treatment inhibited PPARα, downstream gene acyl‐CoA oxidase (ACO), PCNA However, plus 17‐β‐estradiol (10 −8 M) reversed effect induced apoptosis, which was blocked ICI/melatonin/fenofibrate‐treated cells. This illustrates function