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Radiation‐induced HIF‐1α cell survival pathway is inhibited by soy isoflavones in prostate cancer cells by Vinita Singh‐Gupta; Hao Zhang; Sanjeev Banerjee; Dejuan Kong; Julian J. Raffoul; Fazlul H. Sarkar; Gilda G. Hillman is a Medicine article available to read on EtoBox.
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## Abstract We previously showed that treatment of prostate cancer cells with soy isoflavones and radiation resulted in greater cell killing __in vitro,__ and caused downregulation of NF‐κB and APE1/Ref‐1. APE1/Ref‐1 functions as a redox activator of transcription factors, including NF‐κB and HIF‐1α. These molecules are upregulated by radiation and implicated in radioresistance of cancer cells. We extended our studies to investigate the role of HIF‐1α survival pathway and its upstream Src and STAT3 molecules in isoflavones and radiation interaction. Radiation induced phosphorylation of Src and STAT3 leading to induction of HIF‐1α. Genistein, daidzein or a mixture of soy isoflavones did not activate this pathway. These data were observed both in PC‐3 (AR‐) and C4‐2B (AR+) androgen‐independent cell lines. Pretreatment with isoflavones inhibited Src/STAT3/HIF‐1α activation by radiation and nuclear translocation of HIF‐1α. These findings correlated with decreased expression of APE1/Ref‐1 and DNA binding activity of HIF‐1α and NF‐κB. In APE1/Ref‐1 cDNA transfected cells, radiation caused a greater increase in HIF‐1α and NF‐κB activities but this effect was inhibited by pretreatment with
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- Author
- Vinita Singh‐Gupta; Hao Zhang; Sanjeev Banerjee; Dejuan Kong; Julian J. Raffoul; Fazlul H. Sarkar; Gilda G. Hillman
- Publisher
- John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley; Research Square; Test accounts (ISSN 0020-7136)
- Published
- 2009
- Language
- EN
- Field
- Medicine (Health Sciences)