Oxidative stress and castration-resistant prostate cancer

研究成果: Chapter in Book/Report/Conference proceedingChapter

1 被引用数 (Scopus)

抄録

Androgen deprivation therapy can induce oxidative stress by increasing reactive oxygen species levels and/or decreasing cellular antioxidant capacity, which in turn cause genetic and epigenetic effects in prostate cancer. Oxidative stress increases androgen receptor (AR) activation through several possible mechanisms, including AR overexpression, AR activation by co-regulators and intracellular signal transduction pathways, mutation of AR and AR-related proteins, expression of AR splice variants, de novo androgen synthesis, and changes in non-AR signaling. Alterations in AR and non-AR signaling appear to have pro-survival and anti-apoptotic effects on prostate cancer cells, resulting in the development of castration-resistant prostate cancer. Thus, antioxidant therapy could be a promising strategy for the treatment of prostate cancer. Oxidative stress also influences the activity of several prostate cancer therapies, such as taxanes, radiotherapy, and AR-targeting agents. Taken together, these observations suggest that oxidative stress-induced AR signaling is a critical resistance factor and a crucial target for prostate cancer treatment.

本文言語英語
ホスト出版物のタイトルHormone Therapy and Castration Resistance of Prostate Cancer
出版社Springer Singapore
ページ201-214
ページ数14
ISBN(電子版)9789811070136
ISBN(印刷版)9789811070129
DOI
出版ステータス出版済み - 5 11 2018

All Science Journal Classification (ASJC) codes

  • 医学(全般)

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