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A novel antioestrogen agent (3R, 6R)-bassiatin inhibits cell proliferation and cell cycle progression by repressing cyclin D1 expression in 17β-oestradiol-treated MCF-7 cells

Authors

  • Li Meng,

    Corresponding author
    1. Department of Biochemistry and Molecular Biology, Second Military Medical University, 800 Xiangyin Road, Shanghai 200433, Peoples Republic of China
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  • Bo Feng,

    Corresponding author
    1. Department of Biochemistry and Molecular Biology, Second Military Medical University, 800 Xiangyin Road, Shanghai 200433, Peoples Republic of China
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  • Hongwen Tao,

    1. The Key Laboratory of Marine Drugs, Chinese Ministry of Education School of Medicine and Pharmacy, Ocean University of China, Qingdao 266003, Peoples Republic of China
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  • Tingting Yang,

    1. Department of Biochemistry and Molecular Biology, Second Military Medical University, 800 Xiangyin Road, Shanghai 200433, Peoples Republic of China
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  • Yan Meng,

    1. Department of Radiation Oncology, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai 200438, Peoples Republic of China
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  • Weiming Zhu,

    1. The Key Laboratory of Marine Drugs, Chinese Ministry of Education School of Medicine and Pharmacy, Ocean University of China, Qingdao 266003, Peoples Republic of China
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  • Caiguo Huang

    Corresponding author
    1. Department of Biochemistry and Molecular Biology, Second Military Medical University, 800 Xiangyin Road, Shanghai 200433, Peoples Republic of China
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Li Meng and Bo Feng contributed equally to this work.

To whom correspondence should be addressed (email huangcaiguo@hotmail.com).

Abstract

Bassiatin [(3R, 6R)-bassiatin] was isolated from the endogenous fungus Fusarium oxysporum J8-1-2. We found that oestrogen-dependent cell growth was inhibited by bassiatin in MCF-7 ERα (oestrogen receptor α)-positive breast cancer cells. In addition, the mRNA and protein levels of ERα and the oestrogen-responsive gene cyclin D1 were down-regulated by bassiatin in the presence of 17β-oestradiol. Co-treatment of 17β-oestradiol and bassiatin increased phospho-cyclin D1 (Thr286), an indicator of cyclin D1 phosphorylation-dependent degradation. However, this effect was not obvious in the absence of 17β-oestradiol, suggesting that bassiatin may play a role in the metabolism of cyclin D1 by decreasing cyclin D1 protein expression in the presence of 17β-oestradiol. Cyclin D1, known as a key cell cycle regulator, regulates the transition of G1- and S-phase. Decreased cyclin D1 was found to be involved in bassiatin-induced MCF-7 cell cycle arrest. Collectively, our study showed that bassiatin induced cell cycle arrest and exerted an antioestrogen effect. It may prove to be a potential drug target for antioestrogen therapy in ERα-positive breast cancer.

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