Research Project
Grant-in-Aid for Scientific Research (C)
Sustained chronic inflammation and oxidative stress in the prostate promote prostate carcinogenesis. The process of oncogenic transformation leads to enhanced DNA damage and activates the checkpoint network that functions as an inducible barrier against cancer progression. Here, we analyzed the effects of testosterone on the DNA damage response in prostate cancer cells to assess whether testosterone functions a barrier to cancer progression under the oxidative stress. H_2O_2 induced apoptosis and phosphorylation of ATM, Chk2, and H2AX in prostate cancer cells. Androgen treatments increased H_2O_2-induced activation of the DNA damage response and PARP cleavage, but not when the H_2O_2-treated cells were also treated with the anti-androgen flutamide. In this study, we also examined the biological effects of soy isoflavones and curcumin through the DNA damage response in prostate cancer cells. In conclusions, DNA damage response plays important roles in the maintenance of the cell homeostasis in response to oxidative stress during aging. Our results indicate that androgen signaling have tumor suppressive effects in prostate carcinogenesis through DNA damage response pathways under oxidative stress. In addition, our results may indicate that isoflavones and curcumin can modulate serum PSA levels and presumably suppress prostate carcinogenesis through the suppression of androgen receptor expression and the activation of DNA damage signaling pathways.
All 2012 2011 2010
All Journal Article (12 results) (of which Peer Reviewed: 8 results) Presentation (16 results) Book (4 results)
Prostate
Volume: 72 Pages: 1407-11
Korean J Urol
Volume: 53 Pages: 414-8
Asian J Endosc Surg
Volume: 5 Pages: 21-4
Volume: 72 Issue: 13 Pages: 1407-1411
10.1002/pros.22492
Volume: 53 Issue: 6 Pages: 414-418
10.4111/kju.2012.53.6.414
Cancer Sci
Volume: 102 Pages: 468-71
10029290539
Cancer science
Volume: 102 Pages: 468-471
BJU int web site
Cancer Sci.
Volume: 70 Pages: 1127-1133
J Clin Oncol.
Volume: 40 Pages: 815-818
