RNA‐binding protein Musashi2 stabilizing androgen receptor drives prostate cancer progression
The androgen receptor (AR) pathway is critical for prostate cancer carcinogenesis and development; however, after 18‐24 months of AR blocking therapy, patients invariably progress to castration‐resistant prostate cancer (CRPC), which remains an urgent problem to be solved. Therefore, finding key mol...
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| Veröffentlicht in: | Cancer science 2020-02, Vol.111 (2), p.369-382 |
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| creator | Zhao, Jing Zhang, Yu Liu, Xi‐sheng Zhu, Fang‐ming Xie, Feng Jiang, Chen‐yi Zhang, Zi‐ye Gao, Ying‐li Wang, Yong‐chuan Li, Bin Xia, Shu‐jie Han, Bang‐min |
| description | The androgen receptor (AR) pathway is critical for prostate cancer carcinogenesis and development; however, after 18‐24 months of AR blocking therapy, patients invariably progress to castration‐resistant prostate cancer (CRPC), which remains an urgent problem to be solved. Therefore, finding key molecules that interact with AR as novel strategies to treat prostate cancer and even CRPC is desperately needed. In the current study, we focused on the regulation of RNA‐binding proteins (RBPs) associated with AR and determined that the mRNA and protein levels of AR were highly correlated with Musashi2 (MSI2) levels. MSI2 was upregulated in prostate cancer specimens and significantly correlated with advanced tumor grades. Downregulation of MSI2 in both androgen sensitive and insensitive prostate cancer cells inhibited tumor formation in vivo and decreased cell growth in vitro, which could be reversed by AR overexpression. Mechanistically, MSI2 directly bound to the 3′‐untranslated region (UTR) of AR mRNA to increase its stability and, thus, enhanced its transcriptional activity. Our findings illustrate a previously unknown regulatory mechanism in prostate cancer cell proliferation regulated by the MSI2‐AR axis and provide novel evidence towards a strategy against prostate cancer.
This is the first description of a role for the RNA‐binding protein MSI2 in regulating AR stability in prostate cancer. MSI2 upregulates AR mRNA stability through directly binding with 3′‐UTR of AR mRNA, which indicates that targeting MSI2 may be a novel and unique anti–androgen therapy for prostate cancer. |
| doi_str_mv | 10.1111/cas.14280 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7004550</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2351597223</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5330-64254dcf49d467806f55f88169d95b6378f49492774933c44ed769b74f563e1c3</originalsourceid><addsrcrecordid>eNp1kctOAyEUhonRaL0sfAEziSsX03Jn2Jg0jbekauJlTRiGqZiWqTCtqSsfwWf0SaRWjS5kA-T_-M_h_ADsI9hFafWMjl1EcQHXQAcRKnMBIV__PItcQoK3wHaMjxASTiXdBFsEFYRwhDtA3Vz131_fSucr50fZNDStdT67nEUdHxzOYqtLN3YvS1H7KjQj67NgjZ22Tciq4OY2Ll8lrrWZ0d7YsLyPgo3RNX4XbNR6HO3e174D7k9P7gbn-fD67GLQH-aGEQJzTjGjlamprCgXBeQ1Y3VRIC4ryUpORJEkKrEQVBJiKLWV4LIUtGacWGTIDjhe-U5n5cRWxvo26LGaBjfRYaEa7dRfxbsHNWrmKo2KMgaTweGXQWieZja26rGZBZ96VpgwxKTAmCTqaEWZ9OUYbP1TAUG1zEKlLNRnFok9-N3SD_k9_AT0VsCzG9vF_05q0L9dWX4AsY-VBA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2351597223</pqid></control><display><type>article</type><title>RNA‐binding protein Musashi2 stabilizing androgen receptor drives prostate cancer progression</title><source>MEDLINE</source><source>Wiley Online Library Open Access</source><source>DOAJ Directory of Open Access Journals</source><source>Wiley Online Library Journals Frontfile Complete</source><source>PubMed Central</source><creator>Zhao, Jing ; Zhang, Yu ; Liu, Xi‐sheng ; Zhu, Fang‐ming ; Xie, Feng ; Jiang, Chen‐yi ; Zhang, Zi‐ye ; Gao, Ying‐li ; Wang, Yong‐chuan ; Li, Bin ; Xia, Shu‐jie ; Han, Bang‐min</creator><creatorcontrib>Zhao, Jing ; Zhang, Yu ; Liu, Xi‐sheng ; Zhu, Fang‐ming ; Xie, Feng ; Jiang, Chen‐yi ; Zhang, Zi‐ye ; Gao, Ying‐li ; Wang, Yong‐chuan ; Li, Bin ; Xia, Shu‐jie ; Han, Bang‐min</creatorcontrib><description>The androgen receptor (AR) pathway is critical for prostate cancer carcinogenesis and development; however, after 18‐24 months of AR blocking therapy, patients invariably progress to castration‐resistant prostate cancer (CRPC), which remains an urgent problem to be solved. Therefore, finding key molecules that interact with AR as novel strategies to treat prostate cancer and even CRPC is desperately needed. In the current study, we focused on the regulation of RNA‐binding proteins (RBPs) associated with AR and determined that the mRNA and protein levels of AR were highly correlated with Musashi2 (MSI2) levels. MSI2 was upregulated in prostate cancer specimens and significantly correlated with advanced tumor grades. Downregulation of MSI2 in both androgen sensitive and insensitive prostate cancer cells inhibited tumor formation in vivo and decreased cell growth in vitro, which could be reversed by AR overexpression. Mechanistically, MSI2 directly bound to the 3′‐untranslated region (UTR) of AR mRNA to increase its stability and, thus, enhanced its transcriptional activity. Our findings illustrate a previously unknown regulatory mechanism in prostate cancer cell proliferation regulated by the MSI2‐AR axis and provide novel evidence towards a strategy against prostate cancer.
This is the first description of a role for the RNA‐binding protein MSI2 in regulating AR stability in prostate cancer. MSI2 upregulates AR mRNA stability through directly binding with 3′‐UTR of AR mRNA, which indicates that targeting MSI2 may be a novel and unique anti–androgen therapy for prostate cancer.</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/cas.14280</identifier><identifier>PMID: 31833612</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>3' Untranslated Regions ; androgen receptor ; Androgen receptors ; Androgens ; Animals ; Binding sites ; Carcinogenesis ; Castration ; Cell growth ; Cell Line, Tumor ; Cell proliferation ; Disease Progression ; Experiments ; Gene expression ; Gene Expression Regulation, Neoplastic ; Humans ; Immunoglobulins ; Male ; Mice ; Mortality ; mRNA stability ; Musashi2 ; Neoplasm Grading ; Neoplasm Transplantation ; novel anti–androgen therapy ; Original ; Plasmids ; Prostate cancer ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; Protein expression ; Proteins ; Receptors, Androgen - chemistry ; Receptors, Androgen - genetics ; Receptors, Androgen - metabolism ; RNA Stability ; RNA-binding protein ; RNA-Binding Proteins - metabolism ; Transcription ; Up-Regulation</subject><ispartof>Cancer science, 2020-02, Vol.111 (2), p.369-382</ispartof><rights>2019 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2019 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2020. This work is published under http://creativecommons.org/licenses/by-nc-nd/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5330-64254dcf49d467806f55f88169d95b6378f49492774933c44ed769b74f563e1c3</citedby><cites>FETCH-LOGICAL-c5330-64254dcf49d467806f55f88169d95b6378f49492774933c44ed769b74f563e1c3</cites><orcidid>0000-0001-9101-8377</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7004550/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7004550/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,1411,11541,27901,27902,45550,45551,46027,46451,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31833612$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhao, Jing</creatorcontrib><creatorcontrib>Zhang, Yu</creatorcontrib><creatorcontrib>Liu, Xi‐sheng</creatorcontrib><creatorcontrib>Zhu, Fang‐ming</creatorcontrib><creatorcontrib>Xie, Feng</creatorcontrib><creatorcontrib>Jiang, Chen‐yi</creatorcontrib><creatorcontrib>Zhang, Zi‐ye</creatorcontrib><creatorcontrib>Gao, Ying‐li</creatorcontrib><creatorcontrib>Wang, Yong‐chuan</creatorcontrib><creatorcontrib>Li, Bin</creatorcontrib><creatorcontrib>Xia, Shu‐jie</creatorcontrib><creatorcontrib>Han, Bang‐min</creatorcontrib><title>RNA‐binding protein Musashi2 stabilizing androgen receptor drives prostate cancer progression</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>The androgen receptor (AR) pathway is critical for prostate cancer carcinogenesis and development; however, after 18‐24 months of AR blocking therapy, patients invariably progress to castration‐resistant prostate cancer (CRPC), which remains an urgent problem to be solved. Therefore, finding key molecules that interact with AR as novel strategies to treat prostate cancer and even CRPC is desperately needed. In the current study, we focused on the regulation of RNA‐binding proteins (RBPs) associated with AR and determined that the mRNA and protein levels of AR were highly correlated with Musashi2 (MSI2) levels. MSI2 was upregulated in prostate cancer specimens and significantly correlated with advanced tumor grades. Downregulation of MSI2 in both androgen sensitive and insensitive prostate cancer cells inhibited tumor formation in vivo and decreased cell growth in vitro, which could be reversed by AR overexpression. Mechanistically, MSI2 directly bound to the 3′‐untranslated region (UTR) of AR mRNA to increase its stability and, thus, enhanced its transcriptional activity. Our findings illustrate a previously unknown regulatory mechanism in prostate cancer cell proliferation regulated by the MSI2‐AR axis and provide novel evidence towards a strategy against prostate cancer.
This is the first description of a role for the RNA‐binding protein MSI2 in regulating AR stability in prostate cancer. MSI2 upregulates AR mRNA stability through directly binding with 3′‐UTR of AR mRNA, which indicates that targeting MSI2 may be a novel and unique anti–androgen therapy for prostate cancer.</description><subject>3' Untranslated Regions</subject><subject>androgen receptor</subject><subject>Androgen receptors</subject><subject>Androgens</subject><subject>Animals</subject><subject>Binding sites</subject><subject>Carcinogenesis</subject><subject>Castration</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell proliferation</subject><subject>Disease Progression</subject><subject>Experiments</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Immunoglobulins</subject><subject>Male</subject><subject>Mice</subject><subject>Mortality</subject><subject>mRNA stability</subject><subject>Musashi2</subject><subject>Neoplasm Grading</subject><subject>Neoplasm Transplantation</subject><subject>novel anti–androgen therapy</subject><subject>Original</subject><subject>Plasmids</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Receptors, Androgen - chemistry</subject><subject>Receptors, Androgen - genetics</subject><subject>Receptors, Androgen - metabolism</subject><subject>RNA Stability</subject><subject>RNA-binding protein</subject><subject>RNA-Binding Proteins - metabolism</subject><subject>Transcription</subject><subject>Up-Regulation</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kctOAyEUhonRaL0sfAEziSsX03Jn2Jg0jbekauJlTRiGqZiWqTCtqSsfwWf0SaRWjS5kA-T_-M_h_ADsI9hFafWMjl1EcQHXQAcRKnMBIV__PItcQoK3wHaMjxASTiXdBFsEFYRwhDtA3Vz131_fSucr50fZNDStdT67nEUdHxzOYqtLN3YvS1H7KjQj67NgjZ22Tciq4OY2Ll8lrrWZ0d7YsLyPgo3RNX4XbNR6HO3e174D7k9P7gbn-fD67GLQH-aGEQJzTjGjlamprCgXBeQ1Y3VRIC4ryUpORJEkKrEQVBJiKLWV4LIUtGacWGTIDjhe-U5n5cRWxvo26LGaBjfRYaEa7dRfxbsHNWrmKo2KMgaTweGXQWieZja26rGZBZ96VpgwxKTAmCTqaEWZ9OUYbP1TAUG1zEKlLNRnFok9-N3SD_k9_AT0VsCzG9vF_05q0L9dWX4AsY-VBA</recordid><startdate>202002</startdate><enddate>202002</enddate><creator>Zhao, Jing</creator><creator>Zhang, Yu</creator><creator>Liu, Xi‐sheng</creator><creator>Zhu, Fang‐ming</creator><creator>Xie, Feng</creator><creator>Jiang, Chen‐yi</creator><creator>Zhang, Zi‐ye</creator><creator>Gao, Ying‐li</creator><creator>Wang, Yong‐chuan</creator><creator>Li, Bin</creator><creator>Xia, Shu‐jie</creator><creator>Han, Bang‐min</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8FE</scope><scope>8FH</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>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-9101-8377</orcidid></search><sort><creationdate>202002</creationdate><title>RNA‐binding protein Musashi2 stabilizing androgen receptor drives prostate cancer progression</title><author>Zhao, Jing ; Zhang, Yu ; Liu, Xi‐sheng ; Zhu, Fang‐ming ; Xie, Feng ; Jiang, Chen‐yi ; Zhang, Zi‐ye ; Gao, Ying‐li ; Wang, Yong‐chuan ; Li, Bin ; Xia, Shu‐jie ; Han, Bang‐min</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5330-64254dcf49d467806f55f88169d95b6378f49492774933c44ed769b74f563e1c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>3' Untranslated Regions</topic><topic>androgen receptor</topic><topic>Androgen receptors</topic><topic>Androgens</topic><topic>Animals</topic><topic>Binding sites</topic><topic>Carcinogenesis</topic><topic>Castration</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell proliferation</topic><topic>Disease Progression</topic><topic>Experiments</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Immunoglobulins</topic><topic>Male</topic><topic>Mice</topic><topic>Mortality</topic><topic>mRNA stability</topic><topic>Musashi2</topic><topic>Neoplasm Grading</topic><topic>Neoplasm Transplantation</topic><topic>novel anti–androgen therapy</topic><topic>Original</topic><topic>Plasmids</topic><topic>Prostate cancer</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Receptors, Androgen - chemistry</topic><topic>Receptors, Androgen - genetics</topic><topic>Receptors, Androgen - metabolism</topic><topic>RNA Stability</topic><topic>RNA-binding protein</topic><topic>RNA-Binding Proteins - metabolism</topic><topic>Transcription</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhao, Jing</creatorcontrib><creatorcontrib>Zhang, Yu</creatorcontrib><creatorcontrib>Liu, Xi‐sheng</creatorcontrib><creatorcontrib>Zhu, Fang‐ming</creatorcontrib><creatorcontrib>Xie, Feng</creatorcontrib><creatorcontrib>Jiang, Chen‐yi</creatorcontrib><creatorcontrib>Zhang, Zi‐ye</creatorcontrib><creatorcontrib>Gao, Ying‐li</creatorcontrib><creatorcontrib>Wang, Yong‐chuan</creatorcontrib><creatorcontrib>Li, Bin</creatorcontrib><creatorcontrib>Xia, Shu‐jie</creatorcontrib><creatorcontrib>Han, Bang‐min</creatorcontrib><collection>Wiley Online Library Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</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>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhao, Jing</au><au>Zhang, Yu</au><au>Liu, Xi‐sheng</au><au>Zhu, Fang‐ming</au><au>Xie, Feng</au><au>Jiang, Chen‐yi</au><au>Zhang, Zi‐ye</au><au>Gao, Ying‐li</au><au>Wang, Yong‐chuan</au><au>Li, Bin</au><au>Xia, Shu‐jie</au><au>Han, Bang‐min</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>RNA‐binding protein Musashi2 stabilizing androgen receptor drives prostate cancer progression</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2020-02</date><risdate>2020</risdate><volume>111</volume><issue>2</issue><spage>369</spage><epage>382</epage><pages>369-382</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>The androgen receptor (AR) pathway is critical for prostate cancer carcinogenesis and development; however, after 18‐24 months of AR blocking therapy, patients invariably progress to castration‐resistant prostate cancer (CRPC), which remains an urgent problem to be solved. Therefore, finding key molecules that interact with AR as novel strategies to treat prostate cancer and even CRPC is desperately needed. In the current study, we focused on the regulation of RNA‐binding proteins (RBPs) associated with AR and determined that the mRNA and protein levels of AR were highly correlated with Musashi2 (MSI2) levels. MSI2 was upregulated in prostate cancer specimens and significantly correlated with advanced tumor grades. Downregulation of MSI2 in both androgen sensitive and insensitive prostate cancer cells inhibited tumor formation in vivo and decreased cell growth in vitro, which could be reversed by AR overexpression. Mechanistically, MSI2 directly bound to the 3′‐untranslated region (UTR) of AR mRNA to increase its stability and, thus, enhanced its transcriptional activity. Our findings illustrate a previously unknown regulatory mechanism in prostate cancer cell proliferation regulated by the MSI2‐AR axis and provide novel evidence towards a strategy against prostate cancer.
This is the first description of a role for the RNA‐binding protein MSI2 in regulating AR stability in prostate cancer. MSI2 upregulates AR mRNA stability through directly binding with 3′‐UTR of AR mRNA, which indicates that targeting MSI2 may be a novel and unique anti–androgen therapy for prostate cancer.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>31833612</pmid><doi>10.1111/cas.14280</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0001-9101-8377</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 3' Untranslated Regions androgen receptor Androgen receptors Androgens Animals Binding sites Carcinogenesis Castration Cell growth Cell Line, Tumor Cell proliferation Disease Progression Experiments Gene expression Gene Expression Regulation, Neoplastic Humans Immunoglobulins Male Mice Mortality mRNA stability Musashi2 Neoplasm Grading Neoplasm Transplantation novel anti–androgen therapy Original Plasmids Prostate cancer Prostatic Neoplasms - genetics Prostatic Neoplasms - metabolism Prostatic Neoplasms - pathology Protein expression Proteins Receptors, Androgen - chemistry Receptors, Androgen - genetics Receptors, Androgen - metabolism RNA Stability RNA-binding protein RNA-Binding Proteins - metabolism Transcription Up-Regulation |
| title | RNA‐binding protein Musashi2 stabilizing androgen receptor drives prostate cancer progression |
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