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AB070. Roles and mechanisms of soybean isoflavones in androgen-independent transformation of prostate cancer
Author(s) -
Li Xu,
Zhigang Cao,
Yemin Xue,
Shuli Zhao,
Kai Wang,
Chao Jiang,
Qichao Chen
Publication year - 2017
Publication title -
translational andrology and urology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.721
H-Index - 27
eISSN - 2223-4691
pISSN - 2223-4683
DOI - 10.21037/tau.2017.s070
Subject(s) - prostate cancer , isoflavones , transformation (genetics) , androgen receptor , androgen , cancer , cancer research , medicine , chemistry , biochemistry , hormone , gene
The aims of this study were to investigate the impact of soybean isoflavones (SIFs) on the cellular oxidative stress levels in hormone-sensitive type (LNCap) and hormone-insensitive type (DU145) of prostate cancer, and to elucidate the main components and their roles in the transformation of androgen dependency (AD)/androgen independency (AI). The LNCap and DU145 cells were treated with different concentrations of SIFs monomer (including daidzin, genistin, daidzein, and genistein), and the activities of superoxide dismutase (SOD) and malondialdehyde (MDA) were then measured. The content of reactive oxygen species (ROS) in these two cells was also determined after treated with certain effective monomer. The contents of MDA in the two kinds of cells treated with genistein and daidzein were increased, but the contents of SOD were decreased in a concentration-dependent manner. There was no significant difference between daidzin and genistin. The content of MDA in the DU145 cells was higher than that in the LNCap cells under the same conditions, but the content of SOD was decreased, indicating that the oxidative stress level in DU-145 was higher than LNCap, and the ROS level in DU145 treated with effective component was significantly higher than that in LNCap. Genistein and daidzein in SIFs can affect the apoptosis and proliferation of prostate cancer cells through increasing their oxidative stress levels, thus inhibit the transformation of prostate cancer toward androgen-independent type.

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