Non-Coding RNAs in Castration-Resistant Prostate Cancer: Regulation of Androgen Receptor Signaling and Cancer Metabolism

Hormone-refractory prostate cancer frequently relapses from therapy and inevitably progresses to a bone-metastatic status with no cure. Understanding of the molecular mechanisms conferring resistance to androgen deprivation therapy has the potential to lead to the discovery of novel therapeutic targ...

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Main Authors: Jing-Wen Shih, Ling-Yu Wang, Chiu-Lien Hung, Hsing-Jien Kung, Chia-Ling Hsieh
Format: Article
Language:English
Published: MDPI AG 2015-12-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:http://www.mdpi.com/1422-0067/16/12/26138
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spelling doaj-ac195ba9bf514512b573e7a012e156872020-11-24T20:43:47ZengMDPI AGInternational Journal of Molecular Sciences1422-00672015-12-011612289432897810.3390/ijms161226138ijms161226138Non-Coding RNAs in Castration-Resistant Prostate Cancer: Regulation of Androgen Receptor Signaling and Cancer MetabolismJing-Wen Shih0Ling-Yu Wang1Chiu-Lien Hung2Hsing-Jien Kung3Chia-Ling Hsieh4Integrated Translational Lab, The Center of Translational Medicine, Taipei Medical University, Taipei 11031, TaiwanDepartment of Biochemistry and Molecular Medicine, Comprehensive Cancer Center, University of California at Davis, Sacramento, CA 95817, USADepartment of Biochemistry and Molecular Medicine, Comprehensive Cancer Center, University of California at Davis, Sacramento, CA 95817, USAIntegrated Translational Lab, The Center of Translational Medicine, Taipei Medical University, Taipei 11031, TaiwanThe Ph.D. Program for Translational Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei 11031, TaiwanHormone-refractory prostate cancer frequently relapses from therapy and inevitably progresses to a bone-metastatic status with no cure. Understanding of the molecular mechanisms conferring resistance to androgen deprivation therapy has the potential to lead to the discovery of novel therapeutic targets for type of prostate cancer with poor prognosis. Progression to castration-resistant prostate cancer (CRPC) is characterized by aberrant androgen receptor (AR) expression and persistent AR signaling activity. Alterations in metabolic activity regulated by oncogenic pathways, such as c-Myc, were found to promote prostate cancer growth during the development of CRPC. Non-coding RNAs represent a diverse family of regulatory transcripts that drive tumorigenesis of prostate cancer and various other cancers by their hyperactivity or diminished function. A number of studies have examined differentially expressed non-coding RNAs in each stage of prostate cancer. Herein, we highlight the emerging impacts of microRNAs and long non-coding RNAs linked to reactivation of the AR signaling axis and reprogramming of the cellular metabolism in prostate cancer. The translational implications of non-coding RNA research for developing new biomarkers and therapeutic strategies for CRPC are also discussed.http://www.mdpi.com/1422-0067/16/12/26138non-coding RNAmicro RNAslong non-coding RNAscastration-resistant prostate cancerandrogen receptorcancer metabolism
collection DOAJ
language English
format Article
sources DOAJ
author Jing-Wen Shih
Ling-Yu Wang
Chiu-Lien Hung
Hsing-Jien Kung
Chia-Ling Hsieh
spellingShingle Jing-Wen Shih
Ling-Yu Wang
Chiu-Lien Hung
Hsing-Jien Kung
Chia-Ling Hsieh
Non-Coding RNAs in Castration-Resistant Prostate Cancer: Regulation of Androgen Receptor Signaling and Cancer Metabolism
International Journal of Molecular Sciences
non-coding RNA
micro RNAs
long non-coding RNAs
castration-resistant prostate cancer
androgen receptor
cancer metabolism
author_facet Jing-Wen Shih
Ling-Yu Wang
Chiu-Lien Hung
Hsing-Jien Kung
Chia-Ling Hsieh
author_sort Jing-Wen Shih
title Non-Coding RNAs in Castration-Resistant Prostate Cancer: Regulation of Androgen Receptor Signaling and Cancer Metabolism
title_short Non-Coding RNAs in Castration-Resistant Prostate Cancer: Regulation of Androgen Receptor Signaling and Cancer Metabolism
title_full Non-Coding RNAs in Castration-Resistant Prostate Cancer: Regulation of Androgen Receptor Signaling and Cancer Metabolism
title_fullStr Non-Coding RNAs in Castration-Resistant Prostate Cancer: Regulation of Androgen Receptor Signaling and Cancer Metabolism
title_full_unstemmed Non-Coding RNAs in Castration-Resistant Prostate Cancer: Regulation of Androgen Receptor Signaling and Cancer Metabolism
title_sort non-coding rnas in castration-resistant prostate cancer: regulation of androgen receptor signaling and cancer metabolism
publisher MDPI AG
series International Journal of Molecular Sciences
issn 1422-0067
publishDate 2015-12-01
description Hormone-refractory prostate cancer frequently relapses from therapy and inevitably progresses to a bone-metastatic status with no cure. Understanding of the molecular mechanisms conferring resistance to androgen deprivation therapy has the potential to lead to the discovery of novel therapeutic targets for type of prostate cancer with poor prognosis. Progression to castration-resistant prostate cancer (CRPC) is characterized by aberrant androgen receptor (AR) expression and persistent AR signaling activity. Alterations in metabolic activity regulated by oncogenic pathways, such as c-Myc, were found to promote prostate cancer growth during the development of CRPC. Non-coding RNAs represent a diverse family of regulatory transcripts that drive tumorigenesis of prostate cancer and various other cancers by their hyperactivity or diminished function. A number of studies have examined differentially expressed non-coding RNAs in each stage of prostate cancer. Herein, we highlight the emerging impacts of microRNAs and long non-coding RNAs linked to reactivation of the AR signaling axis and reprogramming of the cellular metabolism in prostate cancer. The translational implications of non-coding RNA research for developing new biomarkers and therapeutic strategies for CRPC are also discussed.
topic non-coding RNA
micro RNAs
long non-coding RNAs
castration-resistant prostate cancer
androgen receptor
cancer metabolism
url http://www.mdpi.com/1422-0067/16/12/26138
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