The Crucial Role of AR-V7 in Enzalutamide-Resistance of Castration-Resistant Prostate Cancer
Prostate cancer (PCa) has the second highest incidence of malignancies occurring in men worldwide. The first-line therapy of PCa is androgen deprivation therapy (ADT). Nonetheless, most patients progress to castration-resistant prostate cancer (CRPC) after being treated by ADT. As a second-generatio...
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| Veröffentlicht in: | Cancers 2022-10, Vol.14 (19), p.4877 |
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| creator | Zheng, Zeyuan Li, Jinxin Liu, Yankuo Shi, Zhiyuan Xuan, Zuodong Yang, Kunao Xu, Chunlan Bai, Yang Fu, Meiling Xiao, Qiaohong Sun, Huimin Shao, Chen |
| description | Prostate cancer (PCa) has the second highest incidence of malignancies occurring in men worldwide. The first-line therapy of PCa is androgen deprivation therapy (ADT). Nonetheless, most patients progress to castration-resistant prostate cancer (CRPC) after being treated by ADT. As a second-generation androgen receptor (AR) antagonist, enzalutamide (ENZ) is the current mainstay of new endocrine therapies for CRPC in clinical use. However, almost all patients develop resistance during AR antagonist therapy due to various mechanisms. At present, ENZ resistance (ENZR) has become challenging in the clinical treatment of CRPC. AR splice variant 7 (AR-V7) refers to a ligand-independent and constitutively active variant of the AR and is considered a key driver of ENZR in CRPC. In this review, we summarize the mechanisms and biological behaviors of AR-V7 in ENZR of CRPC to contribute novel insights for CRPC therapy. |
| doi_str_mv | 10.3390/cancers14194877 |
| format | Article |
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The first-line therapy of PCa is androgen deprivation therapy (ADT). Nonetheless, most patients progress to castration-resistant prostate cancer (CRPC) after being treated by ADT. As a second-generation androgen receptor (AR) antagonist, enzalutamide (ENZ) is the current mainstay of new endocrine therapies for CRPC in clinical use. However, almost all patients develop resistance during AR antagonist therapy due to various mechanisms. At present, ENZ resistance (ENZR) has become challenging in the clinical treatment of CRPC. AR splice variant 7 (AR-V7) refers to a ligand-independent and constitutively active variant of the AR and is considered a key driver of ENZR in CRPC. In this review, we summarize the mechanisms and biological behaviors of AR-V7 in ENZR of CRPC to contribute novel insights for CRPC therapy.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers14194877</identifier><identifier>PMID: 36230800</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Alternative splicing ; Androgen receptors ; Androgens ; Binding sites ; Cancer therapies ; Castration ; Drug resistance ; Drug therapy ; Endocrine therapy ; FDA approval ; Genes ; Genetic aspects ; Health aspects ; Homeostasis ; Ligands ; Messenger RNA ; Metastasis ; Mutation ; Non-coding RNA ; Patients ; Prostate cancer ; Proteins ; Review</subject><ispartof>Cancers, 2022-10, Vol.14 (19), p.4877</ispartof><rights>COPYRIGHT 2022 MDPI AG</rights><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). 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The first-line therapy of PCa is androgen deprivation therapy (ADT). Nonetheless, most patients progress to castration-resistant prostate cancer (CRPC) after being treated by ADT. As a second-generation androgen receptor (AR) antagonist, enzalutamide (ENZ) is the current mainstay of new endocrine therapies for CRPC in clinical use. However, almost all patients develop resistance during AR antagonist therapy due to various mechanisms. At present, ENZ resistance (ENZR) has become challenging in the clinical treatment of CRPC. AR splice variant 7 (AR-V7) refers to a ligand-independent and constitutively active variant of the AR and is considered a key driver of ENZR in CRPC. In this review, we summarize the mechanisms and biological behaviors of AR-V7 in ENZR of CRPC to contribute novel insights for CRPC therapy.</description><subject>Alternative splicing</subject><subject>Androgen receptors</subject><subject>Androgens</subject><subject>Binding sites</subject><subject>Cancer therapies</subject><subject>Castration</subject><subject>Drug resistance</subject><subject>Drug therapy</subject><subject>Endocrine therapy</subject><subject>FDA approval</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Homeostasis</subject><subject>Ligands</subject><subject>Messenger RNA</subject><subject>Metastasis</subject><subject>Mutation</subject><subject>Non-coding RNA</subject><subject>Patients</subject><subject>Prostate cancer</subject><subject>Proteins</subject><subject>Review</subject><issn>2072-6694</issn><issn>2072-6694</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkkFLHTEQx0OpVFHPvS700stqkskmm0vh8bCtILQ8bE-FkM3OamQ3scmu0H76ZlVslSaHDDO_-c9MGELeMnoCoOmps8FhykwwLVqlXpEDThWvpdTi9T_2PjnO-YaWA8CUVG_IPkgOtKX0gPy4vMZqmxbn7Vjt4ohVHKrNrv6uKh-qs_DbjstsJ99jvcPs87zWXJmtzXOys4_hKTBXX1MsxlwU71s7InuDHTMeP76H5NvHs8vt5_riy6fz7eaidqCbue601IyjGJRs3KBVB9Datu1UZ7FxaLVzUst-6HSZEnjTC2qZa_uBQde41sEh-fCge7t0E_YOQ2ltNLfJTzb9MtF68zwS_LW5indGNxK4gCLw_lEgxZ8L5tlMPjscRxswLtlwxRumQYEo6LsX6E1cUijjrZTgwICrv9SVHdH4MMRS162iZqNEwxXTqi3UyX-ocnucvIsBB1_8zxJOHxJc-eiccHiakVGz7oR5sRPwB4meqKc</recordid><startdate>20221005</startdate><enddate>20221005</enddate><creator>Zheng, Zeyuan</creator><creator>Li, Jinxin</creator><creator>Liu, Yankuo</creator><creator>Shi, Zhiyuan</creator><creator>Xuan, Zuodong</creator><creator>Yang, Kunao</creator><creator>Xu, Chunlan</creator><creator>Bai, Yang</creator><creator>Fu, Meiling</creator><creator>Xiao, Qiaohong</creator><creator>Sun, Huimin</creator><creator>Shao, Chen</creator><general>MDPI AG</general><general>MDPI</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-9935-5631</orcidid></search><sort><creationdate>20221005</creationdate><title>The Crucial Role of AR-V7 in Enzalutamide-Resistance of Castration-Resistant Prostate Cancer</title><author>Zheng, Zeyuan ; Li, Jinxin ; Liu, Yankuo ; Shi, Zhiyuan ; Xuan, Zuodong ; Yang, Kunao ; Xu, Chunlan ; Bai, Yang ; Fu, Meiling ; Xiao, Qiaohong ; Sun, Huimin ; Shao, Chen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c395t-b96912e4f765cf97b338a88b7bae5cea9cc696dfb9877325d40a1c8df13b5c8c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Alternative splicing</topic><topic>Androgen receptors</topic><topic>Androgens</topic><topic>Binding sites</topic><topic>Cancer therapies</topic><topic>Castration</topic><topic>Drug resistance</topic><topic>Drug therapy</topic><topic>Endocrine therapy</topic><topic>FDA approval</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Homeostasis</topic><topic>Ligands</topic><topic>Messenger RNA</topic><topic>Metastasis</topic><topic>Mutation</topic><topic>Non-coding RNA</topic><topic>Patients</topic><topic>Prostate cancer</topic><topic>Proteins</topic><topic>Review</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zheng, Zeyuan</creatorcontrib><creatorcontrib>Li, Jinxin</creatorcontrib><creatorcontrib>Liu, Yankuo</creatorcontrib><creatorcontrib>Shi, Zhiyuan</creatorcontrib><creatorcontrib>Xuan, Zuodong</creatorcontrib><creatorcontrib>Yang, Kunao</creatorcontrib><creatorcontrib>Xu, Chunlan</creatorcontrib><creatorcontrib>Bai, Yang</creatorcontrib><creatorcontrib>Fu, Meiling</creatorcontrib><creatorcontrib>Xiao, Qiaohong</creatorcontrib><creatorcontrib>Sun, Huimin</creatorcontrib><creatorcontrib>Shao, Chen</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancers</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zheng, Zeyuan</au><au>Li, Jinxin</au><au>Liu, Yankuo</au><au>Shi, Zhiyuan</au><au>Xuan, Zuodong</au><au>Yang, Kunao</au><au>Xu, Chunlan</au><au>Bai, Yang</au><au>Fu, Meiling</au><au>Xiao, Qiaohong</au><au>Sun, Huimin</au><au>Shao, Chen</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Crucial Role of AR-V7 in Enzalutamide-Resistance of Castration-Resistant Prostate Cancer</atitle><jtitle>Cancers</jtitle><date>2022-10-05</date><risdate>2022</risdate><volume>14</volume><issue>19</issue><spage>4877</spage><pages>4877-</pages><issn>2072-6694</issn><eissn>2072-6694</eissn><abstract>Prostate cancer (PCa) has the second highest incidence of malignancies occurring in men worldwide. The first-line therapy of PCa is androgen deprivation therapy (ADT). Nonetheless, most patients progress to castration-resistant prostate cancer (CRPC) after being treated by ADT. As a second-generation androgen receptor (AR) antagonist, enzalutamide (ENZ) is the current mainstay of new endocrine therapies for CRPC in clinical use. However, almost all patients develop resistance during AR antagonist therapy due to various mechanisms. At present, ENZ resistance (ENZR) has become challenging in the clinical treatment of CRPC. AR splice variant 7 (AR-V7) refers to a ligand-independent and constitutively active variant of the AR and is considered a key driver of ENZR in CRPC. In this review, we summarize the mechanisms and biological behaviors of AR-V7 in ENZR of CRPC to contribute novel insights for CRPC therapy.</abstract><cop>Basel</cop><pub>MDPI AG</pub><pmid>36230800</pmid><doi>10.3390/cancers14194877</doi><orcidid>https://orcid.org/0000-0002-9935-5631</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; PubMed Central Open Access |
| subjects | Alternative splicing Androgen receptors Androgens Binding sites Cancer therapies Castration Drug resistance Drug therapy Endocrine therapy FDA approval Genes Genetic aspects Health aspects Homeostasis Ligands Messenger RNA Metastasis Mutation Non-coding RNA Patients Prostate cancer Proteins Review |
| title | The Crucial Role of AR-V7 in Enzalutamide-Resistance of Castration-Resistant Prostate Cancer |
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