Oxidative stress and castration-resistant prostate cancer

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

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.

Original languageEnglish
Title of host publicationHormone Therapy and Castration Resistance of Prostate Cancer
PublisherSpringer Singapore
Pages201-214
Number of pages14
ISBN (Electronic)9789811070136
ISBN (Print)9789811070129
DOIs
Publication statusPublished - May 11 2018

Fingerprint

Castration
Androgen Receptors
Prostatic Neoplasms
Oxidative Stress
Androgens
Antioxidants
Therapeutics
Taxoids
R Factors
Epigenomics
Reactive Oxygen Species
Signal Transduction
Radiotherapy
Mutation

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

shiota, M. (2018). Oxidative stress and castration-resistant prostate cancer. In Hormone Therapy and Castration Resistance of Prostate Cancer (pp. 201-214). Springer Singapore. https://doi.org/10.1007/978-981-10-7013-6_21

Oxidative stress and castration-resistant prostate cancer. / shiota, masaki.

Hormone Therapy and Castration Resistance of Prostate Cancer. Springer Singapore, 2018. p. 201-214.

Research output: Chapter in Book/Report/Conference proceedingChapter

shiota, M 2018, Oxidative stress and castration-resistant prostate cancer. in Hormone Therapy and Castration Resistance of Prostate Cancer. Springer Singapore, pp. 201-214. https://doi.org/10.1007/978-981-10-7013-6_21
shiota M. Oxidative stress and castration-resistant prostate cancer. In Hormone Therapy and Castration Resistance of Prostate Cancer. Springer Singapore. 2018. p. 201-214 https://doi.org/10.1007/978-981-10-7013-6_21
shiota, masaki. / Oxidative stress and castration-resistant prostate cancer. Hormone Therapy and Castration Resistance of Prostate Cancer. Springer Singapore, 2018. pp. 201-214
@inbook{8a99aeff5b3e406bad8f8c52bf490b1f,
title = "Oxidative stress and castration-resistant prostate cancer",
abstract = "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.",
author = "masaki shiota",
year = "2018",
month = "5",
day = "11",
doi = "10.1007/978-981-10-7013-6_21",
language = "English",
isbn = "9789811070129",
pages = "201--214",
booktitle = "Hormone Therapy and Castration Resistance of Prostate Cancer",
publisher = "Springer Singapore",

}

TY - CHAP

T1 - Oxidative stress and castration-resistant prostate cancer

AU - shiota, masaki

PY - 2018/5/11

Y1 - 2018/5/11

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=85053172593&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85053172593&partnerID=8YFLogxK

U2 - 10.1007/978-981-10-7013-6_21

DO - 10.1007/978-981-10-7013-6_21

M3 - Chapter

AN - SCOPUS:85053172593

SN - 9789811070129

SP - 201

EP - 214

BT - Hormone Therapy and Castration Resistance of Prostate Cancer

PB - Springer Singapore

ER -