GOLM1 promotes prostate cancer progression via interaction with PSMD1 and enhancing AR‐driven transcriptional activation
Aberrant transcriptional activation of the androgen receptor (AR) is a predominant cause of prostate cancer (PCa), including both in the initial and androgen‐independent stages. Our study highlights Golgi membrane protein 1 (GOLM1) as a key regulator of AR‐driven transcriptional activity in PCa prog...
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description | Aberrant transcriptional activation of the androgen receptor (AR) is a predominant cause of prostate cancer (PCa), including both in the initial and androgen‐independent stages. Our study highlights Golgi membrane protein 1 (GOLM1) as a key regulator of AR‐driven transcriptional activity in PCa progression. Utilizing local clinical data and TCGA data, we have established a robust association between GOLM1 and AR target genes, and further demonstrated that GOLM1 can enhance the expression of AR target genes. We discovered that GOLM1 interacts with PSMD1, a component of the 19S regulatory complex in the 26S proteasome, using mass spectrometry and Co‐IP analysis. It is well known that ubiquitin‐proteasome plays a vital role in AR expression and transcriptional regulation. Our findings demonstrate that GOLM1 enhances ubiquitin proteasome activity by binding to PSMD1, thereby facilitating AR‐driven transcriptional activity and PCa progression. These results indicate that GOLM1 and its associated proteins may become potential therapeutic targets for PCa characterized by dysregulated AR‐driven transcriptional activation. |
doi_str_mv | 10.1111/jcmm.70186 |
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Our study highlights Golgi membrane protein 1 (GOLM1) as a key regulator of AR‐driven transcriptional activity in PCa progression. Utilizing local clinical data and TCGA data, we have established a robust association between GOLM1 and AR target genes, and further demonstrated that GOLM1 can enhance the expression of AR target genes. We discovered that GOLM1 interacts with PSMD1, a component of the 19S regulatory complex in the 26S proteasome, using mass spectrometry and Co‐IP analysis. It is well known that ubiquitin‐proteasome plays a vital role in AR expression and transcriptional regulation. Our findings demonstrate that GOLM1 enhances ubiquitin proteasome activity by binding to PSMD1, thereby facilitating AR‐driven transcriptional activity and PCa progression. These results indicate that GOLM1 and its associated proteins may become potential therapeutic targets for PCa characterized by dysregulated AR‐driven transcriptional activation.</description><identifier>ISSN: 1582-1838</identifier><identifier>ISSN: 1582-4934</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.70186</identifier><identifier>PMID: 39470578</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Androgen receptors ; Androgens ; Animals ; Antibodies ; Cell growth ; Cell Line, Tumor ; Correlation analysis ; Disease Progression ; Enzymes ; Gene Expression Regulation, Neoplastic ; Gene regulation ; Golgi apparatus ; GOLM1 ; Humans ; Immunohistochemistry ; Laboratories ; Liver cancer ; Lung cancer ; Male ; Mass spectrometry ; Mass spectroscopy ; Medical research ; Membrane Proteins - genetics ; Membrane Proteins - metabolism ; Mice ; Original ; Prostate cancer ; Prostatic Neoplasms - genetics ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; Proteasome 26S ; Proteasome Endopeptidase Complex - metabolism ; Proteasomes ; Protein Binding ; Proteins ; PSMD1 ; Receptors, Androgen - genetics ; Receptors, Androgen - metabolism ; Scientific imaging ; Survival analysis ; Therapeutic targets ; Transcription activation ; Transcriptional Activation - genetics ; Ubiquitin ; UPS</subject><ispartof>Journal of cellular and molecular medicine, 2024-10, Vol.28 (20), p.e70186-n/a</ispartof><rights>2024 The Author(s). published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2024 The Author(s). Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2024. This work is published under http://creativecommons.org/licenses/by/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><cites>FETCH-LOGICAL-c3386-c0dda416b18cfa72364b17531a8aef7f855899a27fc4b1358287e243f48662bd3</cites><orcidid>0000-0003-3672-8215</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/PMC11520440/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11520440/$$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/39470578$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yan, Guang</creatorcontrib><creatorcontrib>Zhu, Tianhang</creatorcontrib><creatorcontrib>Zhou, Jiawei</creatorcontrib><creatorcontrib>Li, Xia</creatorcontrib><creatorcontrib>Wen, Zonghua</creatorcontrib><creatorcontrib>Miuhuitijiang, Bahaerguli</creatorcontrib><creatorcontrib>Zhang, Zhiyong</creatorcontrib><creatorcontrib>Du, Yuejun</creatorcontrib><creatorcontrib>Li, Chengyao</creatorcontrib><creatorcontrib>Shi, Xiaojun</creatorcontrib><creatorcontrib>Tan, Wanlong</creatorcontrib><title>GOLM1 promotes prostate cancer progression via interaction with PSMD1 and enhancing AR‐driven transcriptional activation</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Aberrant transcriptional activation of the androgen receptor (AR) is a predominant cause of prostate cancer (PCa), including both in the initial and androgen‐independent stages. Our study highlights Golgi membrane protein 1 (GOLM1) as a key regulator of AR‐driven transcriptional activity in PCa progression. Utilizing local clinical data and TCGA data, we have established a robust association between GOLM1 and AR target genes, and further demonstrated that GOLM1 can enhance the expression of AR target genes. We discovered that GOLM1 interacts with PSMD1, a component of the 19S regulatory complex in the 26S proteasome, using mass spectrometry and Co‐IP analysis. It is well known that ubiquitin‐proteasome plays a vital role in AR expression and transcriptional regulation. Our findings demonstrate that GOLM1 enhances ubiquitin proteasome activity by binding to PSMD1, thereby facilitating AR‐driven transcriptional activity and PCa progression. These results indicate that GOLM1 and its associated proteins may become potential therapeutic targets for PCa characterized by dysregulated AR‐driven transcriptional activation.</description><subject>Androgen receptors</subject><subject>Androgens</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Correlation analysis</subject><subject>Disease Progression</subject><subject>Enzymes</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene regulation</subject><subject>Golgi apparatus</subject><subject>GOLM1</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Laboratories</subject><subject>Liver cancer</subject><subject>Lung cancer</subject><subject>Male</subject><subject>Mass spectrometry</subject><subject>Mass spectroscopy</subject><subject>Medical research</subject><subject>Membrane Proteins - genetics</subject><subject>Membrane Proteins - metabolism</subject><subject>Mice</subject><subject>Original</subject><subject>Prostate cancer</subject><subject>Prostatic Neoplasms - genetics</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Proteasome 26S</subject><subject>Proteasome Endopeptidase Complex - metabolism</subject><subject>Proteasomes</subject><subject>Protein Binding</subject><subject>Proteins</subject><subject>PSMD1</subject><subject>Receptors, Androgen - genetics</subject><subject>Receptors, Androgen - metabolism</subject><subject>Scientific imaging</subject><subject>Survival analysis</subject><subject>Therapeutic targets</subject><subject>Transcription activation</subject><subject>Transcriptional Activation - genetics</subject><subject>Ubiquitin</subject><subject>UPS</subject><issn>1582-1838</issn><issn>1582-4934</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kc9u1DAQxq0K1H_0wgMgS1wqpG09sZM4J1RtoVDtqgjo2Zp1nF2vEmdrZ7dqTzxCn7FPgtNsK-CAL57R_ObTzHyEvAV2AvGdLnXTnOQMZLZD9iGVyUgUXLzaxiC53CMHISwZ4xnwYpfs8ULkLM3lPrm_uJpMga5827SdCX0QOuwM1ei08X0-9yYE2zq6sUit64xH3fX5re0W9NuP6TlQdCU1bhF7rJvTs--Pvx5KbzfG0c6jC9rbVd-CNe17N9gnb8jrCutgjrb_Ibn-_Onn-MtocnXxdXw2GWnOZTbSrCxRQDYDqSvME56JGeQpB5RoqrySaSqLApO80rHA48oyN4nglZBZlsxKfkg-Drqr9awxpTYuzlSrlbcN-jvVolV_V5xdqHm7UQBpwoRgUeF4q-Dbm7UJnWps0Kau0Zl2HRSHBNICklRG9P0_6LJd-7j4QMlM8oJH6sNA6Xju4E31Mg0w1Xuqek_Vk6cRfvfn_C_os4kRgAG4tbW5-4-UuhxPp4Pob5m2rxs</recordid><startdate>202410</startdate><enddate>202410</enddate><creator>Yan, Guang</creator><creator>Zhu, Tianhang</creator><creator>Zhou, Jiawei</creator><creator>Li, Xia</creator><creator>Wen, Zonghua</creator><creator>Miuhuitijiang, Bahaerguli</creator><creator>Zhang, Zhiyong</creator><creator>Du, Yuejun</creator><creator>Li, Chengyao</creator><creator>Shi, Xiaojun</creator><creator>Tan, Wanlong</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>3V.</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-3672-8215</orcidid></search><sort><creationdate>202410</creationdate><title>GOLM1 promotes prostate cancer progression via interaction with PSMD1 and enhancing AR‐driven transcriptional activation</title><author>Yan, Guang ; Zhu, Tianhang ; Zhou, Jiawei ; Li, Xia ; Wen, Zonghua ; Miuhuitijiang, Bahaerguli ; Zhang, Zhiyong ; Du, Yuejun ; Li, Chengyao ; Shi, Xiaojun ; Tan, Wanlong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3386-c0dda416b18cfa72364b17531a8aef7f855899a27fc4b1358287e243f48662bd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Androgen receptors</topic><topic>Androgens</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Correlation analysis</topic><topic>Disease Progression</topic><topic>Enzymes</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene regulation</topic><topic>Golgi apparatus</topic><topic>GOLM1</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Laboratories</topic><topic>Liver cancer</topic><topic>Lung cancer</topic><topic>Male</topic><topic>Mass spectrometry</topic><topic>Mass spectroscopy</topic><topic>Medical research</topic><topic>Membrane Proteins - genetics</topic><topic>Membrane Proteins - metabolism</topic><topic>Mice</topic><topic>Original</topic><topic>Prostate cancer</topic><topic>Prostatic Neoplasms - genetics</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Proteasome 26S</topic><topic>Proteasome Endopeptidase Complex - metabolism</topic><topic>Proteasomes</topic><topic>Protein Binding</topic><topic>Proteins</topic><topic>PSMD1</topic><topic>Receptors, Androgen - genetics</topic><topic>Receptors, Androgen - metabolism</topic><topic>Scientific imaging</topic><topic>Survival analysis</topic><topic>Therapeutic targets</topic><topic>Transcription activation</topic><topic>Transcriptional Activation - genetics</topic><topic>Ubiquitin</topic><topic>UPS</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yan, Guang</creatorcontrib><creatorcontrib>Zhu, Tianhang</creatorcontrib><creatorcontrib>Zhou, Jiawei</creatorcontrib><creatorcontrib>Li, Xia</creatorcontrib><creatorcontrib>Wen, Zonghua</creatorcontrib><creatorcontrib>Miuhuitijiang, Bahaerguli</creatorcontrib><creatorcontrib>Zhang, Zhiyong</creatorcontrib><creatorcontrib>Du, Yuejun</creatorcontrib><creatorcontrib>Li, Chengyao</creatorcontrib><creatorcontrib>Shi, Xiaojun</creatorcontrib><creatorcontrib>Tan, Wanlong</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 Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</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>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yan, Guang</au><au>Zhu, Tianhang</au><au>Zhou, Jiawei</au><au>Li, Xia</au><au>Wen, Zonghua</au><au>Miuhuitijiang, Bahaerguli</au><au>Zhang, Zhiyong</au><au>Du, Yuejun</au><au>Li, Chengyao</au><au>Shi, Xiaojun</au><au>Tan, Wanlong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>GOLM1 promotes prostate cancer progression via interaction with PSMD1 and enhancing AR‐driven transcriptional activation</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2024-10</date><risdate>2024</risdate><volume>28</volume><issue>20</issue><spage>e70186</spage><epage>n/a</epage><pages>e70186-n/a</pages><issn>1582-1838</issn><issn>1582-4934</issn><eissn>1582-4934</eissn><abstract>Aberrant transcriptional activation of the androgen receptor (AR) is a predominant cause of prostate cancer (PCa), including both in the initial and androgen‐independent stages. Our study highlights Golgi membrane protein 1 (GOLM1) as a key regulator of AR‐driven transcriptional activity in PCa progression. Utilizing local clinical data and TCGA data, we have established a robust association between GOLM1 and AR target genes, and further demonstrated that GOLM1 can enhance the expression of AR target genes. We discovered that GOLM1 interacts with PSMD1, a component of the 19S regulatory complex in the 26S proteasome, using mass spectrometry and Co‐IP analysis. It is well known that ubiquitin‐proteasome plays a vital role in AR expression and transcriptional regulation. Our findings demonstrate that GOLM1 enhances ubiquitin proteasome activity by binding to PSMD1, thereby facilitating AR‐driven transcriptional activity and PCa progression. These results indicate that GOLM1 and its associated proteins may become potential therapeutic targets for PCa characterized by dysregulated AR‐driven transcriptional activation.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>39470578</pmid><doi>10.1111/jcmm.70186</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0003-3672-8215</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Androgen receptors Androgens Animals Antibodies Cell growth Cell Line, Tumor Correlation analysis Disease Progression Enzymes Gene Expression Regulation, Neoplastic Gene regulation Golgi apparatus GOLM1 Humans Immunohistochemistry Laboratories Liver cancer Lung cancer Male Mass spectrometry Mass spectroscopy Medical research Membrane Proteins - genetics Membrane Proteins - metabolism Mice Original Prostate cancer Prostatic Neoplasms - genetics Prostatic Neoplasms - metabolism Prostatic Neoplasms - pathology Proteasome 26S Proteasome Endopeptidase Complex - metabolism Proteasomes Protein Binding Proteins PSMD1 Receptors, Androgen - genetics Receptors, Androgen - metabolism Scientific imaging Survival analysis Therapeutic targets Transcription activation Transcriptional Activation - genetics Ubiquitin UPS |
title | GOLM1 promotes prostate cancer progression via interaction with PSMD1 and enhancing AR‐driven transcriptional activation |
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