SNHG15 Mediates MTSS1 Gene Expression via Interacting with the Gene Promoter and Regulating Transcription Pausing
Metastasis suppressor 1 (MTSS1) has been reported to play important roles in suppressing cancer progression. In this study, we investigated the underlying mechanism that regulates MTSS1 expression. We showed that in breast cancer cells, lncRNA-SNHG15-induced cell invasion and proliferation was accom...
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| Veröffentlicht in: | International journal of molecular sciences 2024-11, Vol.25 (21), p.11565 |
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| creator | Zhou, Yanchun Chen, Shaoying Chen, Weibin Wu, Jundong Gu, Wei |
| description | Metastasis suppressor 1 (MTSS1) has been reported to play important roles in suppressing cancer progression. In this study, we investigated the underlying mechanism that regulates MTSS1 expression. We showed that in breast cancer cells, lncRNA-SNHG15-induced cell invasion and proliferation was accompanied with the decreased expression of MTSS1 mRNA. Further study revealed that SNHG15 mediated MTSS1 repression through blocking its promoter activity. Mechanistically, SNHG15 complexes with DDX5 and RTF1 and interacts with the core promoter of the MTSS1 gene to interfere with RNA-Pol-II-directed transcriptional initiation. Association with DDX5 stabilizes SNHG15 while binding to RTF1 allows SNHG15 to carry RTF1 to the core promoter, where RTF1 forms a complex with PNA pl II to enhance transcriptional pausing. Our findings revealed a molecular mechanism by which SNHG15 serves as a regulator to suppresses MTSS1 transcription via interaction with the gene core promoter. |
| doi_str_mv | 10.3390/ijms252111565 |
| format | Article |
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In this study, we investigated the underlying mechanism that regulates MTSS1 expression. We showed that in breast cancer cells, lncRNA-SNHG15-induced cell invasion and proliferation was accompanied with the decreased expression of MTSS1 mRNA. Further study revealed that SNHG15 mediated MTSS1 repression through blocking its promoter activity. Mechanistically, SNHG15 complexes with DDX5 and RTF1 and interacts with the core promoter of the MTSS1 gene to interfere with RNA-Pol-II-directed transcriptional initiation. Association with DDX5 stabilizes SNHG15 while binding to RTF1 allows SNHG15 to carry RTF1 to the core promoter, where RTF1 forms a complex with PNA pl II to enhance transcriptional pausing. Our findings revealed a molecular mechanism by which SNHG15 serves as a regulator to suppresses MTSS1 transcription via interaction with the gene core promoter.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms252111565</identifier><identifier>PMID: 39519115</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cell growth ; Cell Line, Tumor ; Cell Proliferation - genetics ; DEAD-box RNA Helicases - genetics ; DEAD-box RNA Helicases - metabolism ; Development and progression ; DNA methylation ; Ethylenediaminetetraacetic acid ; Female ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genes ; Genetic aspects ; Genetic transcription ; Humans ; Mediation ; Messenger RNA ; Metastasis ; Microfilament Proteins - genetics ; Microfilament Proteins - metabolism ; Neoplasm Proteins - genetics ; Neoplasm Proteins - metabolism ; Promoter Regions, Genetic ; Promoters (Genetics) ; Proteins ; RNA polymerase ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Scientific imaging ; Transcription, Genetic ; Tumors</subject><ispartof>International journal of molecular sciences, 2024-11, Vol.25 (21), p.11565</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 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/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2024 by the authors. 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c369t-1798e42caff5a537df3abb9302aec13e4a089c08ad811fdafba4fdc71152fa223</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11546481/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11546481/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39519115$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Yanchun</creatorcontrib><creatorcontrib>Chen, Shaoying</creatorcontrib><creatorcontrib>Chen, Weibin</creatorcontrib><creatorcontrib>Wu, Jundong</creatorcontrib><creatorcontrib>Gu, Wei</creatorcontrib><title>SNHG15 Mediates MTSS1 Gene Expression via Interacting with the Gene Promoter and Regulating Transcription Pausing</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>Metastasis suppressor 1 (MTSS1) has been reported to play important roles in suppressing cancer progression. In this study, we investigated the underlying mechanism that regulates MTSS1 expression. We showed that in breast cancer cells, lncRNA-SNHG15-induced cell invasion and proliferation was accompanied with the decreased expression of MTSS1 mRNA. Further study revealed that SNHG15 mediated MTSS1 repression through blocking its promoter activity. Mechanistically, SNHG15 complexes with DDX5 and RTF1 and interacts with the core promoter of the MTSS1 gene to interfere with RNA-Pol-II-directed transcriptional initiation. Association with DDX5 stabilizes SNHG15 while binding to RTF1 allows SNHG15 to carry RTF1 to the core promoter, where RTF1 forms a complex with PNA pl II to enhance transcriptional pausing. Our findings revealed a molecular mechanism by which SNHG15 serves as a regulator to suppresses MTSS1 transcription via interaction with the gene core promoter.</description><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - genetics</subject><subject>DEAD-box RNA Helicases - genetics</subject><subject>DEAD-box RNA Helicases - metabolism</subject><subject>Development and progression</subject><subject>DNA methylation</subject><subject>Ethylenediaminetetraacetic acid</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic transcription</subject><subject>Humans</subject><subject>Mediation</subject><subject>Messenger RNA</subject><subject>Metastasis</subject><subject>Microfilament Proteins - genetics</subject><subject>Microfilament Proteins - metabolism</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - metabolism</subject><subject>Promoter Regions, Genetic</subject><subject>Promoters (Genetics)</subject><subject>Proteins</subject><subject>RNA polymerase</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Scientific imaging</subject><subject>Transcription, Genetic</subject><subject>Tumors</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptkktvEzEQgFcIRB9w5IosceGyxc_N7glVVUkrtVCRcLYm3nHiaNdO7d1C_z1OU0qDkA-2Zr75RmNNUbxj9ESIhn5y6z5xxRljqlIvikMmOS8prSYvn70PiqOU1pRywVXzujgQjWJNrjgsbmdfL6ZMkWtsHQyYyPV8NmNkih7J-a9NxJRc8OTOAbn0A0Ywg_NL8tMNKzKscAfexNCHnCTgW_Idl2MHD9Q8gk8mus2wddzAmHL0TfHKQpfw7eN9XPz4cj4_uyivvk0vz06vSiOqZijZpKlRcgPWKlBi0loBi0UjKAc0TKAEWjeG1tDWjNkW7AKkbc0kT8UtcC6Oi88772Zc9Nga9EOETm-i6yHe6wBO72e8W-lluNPZICtZs2z4-GiI4XbENOjeJYNdBx7DmLRgvJ5ISZXM6Id_0HUYo8_zbamKKsYq-pdaQofaeRtyY7OV6tOaKSGVfHCd_IfKp8XemeDRuhzfKyh3BSaGlCLapyEZ1dsl0XtLkvn3z3_mif6zFeI37dO3rQ</recordid><startdate>20241101</startdate><enddate>20241101</enddate><creator>Zhou, Yanchun</creator><creator>Chen, Shaoying</creator><creator>Chen, Weibin</creator><creator>Wu, Jundong</creator><creator>Gu, Wei</creator><general>MDPI AG</general><general>MDPI</general><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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</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></search><sort><creationdate>20241101</creationdate><title>SNHG15 Mediates MTSS1 Gene Expression via Interacting with the Gene Promoter and Regulating Transcription Pausing</title><author>Zhou, Yanchun ; Chen, Shaoying ; Chen, Weibin ; Wu, Jundong ; Gu, Wei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c369t-1798e42caff5a537df3abb9302aec13e4a089c08ad811fdafba4fdc71152fa223</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - genetics</topic><topic>DEAD-box RNA Helicases - genetics</topic><topic>DEAD-box RNA Helicases - metabolism</topic><topic>Development and progression</topic><topic>DNA methylation</topic><topic>Ethylenediaminetetraacetic acid</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic transcription</topic><topic>Humans</topic><topic>Mediation</topic><topic>Messenger RNA</topic><topic>Metastasis</topic><topic>Microfilament Proteins - genetics</topic><topic>Microfilament Proteins - metabolism</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - metabolism</topic><topic>Promoter Regions, Genetic</topic><topic>Promoters (Genetics)</topic><topic>Proteins</topic><topic>RNA polymerase</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Scientific imaging</topic><topic>Transcription, Genetic</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Yanchun</creatorcontrib><creatorcontrib>Chen, Shaoying</creatorcontrib><creatorcontrib>Chen, Weibin</creatorcontrib><creatorcontrib>Wu, Jundong</creatorcontrib><creatorcontrib>Gu, Wei</creatorcontrib><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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</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>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</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>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Yanchun</au><au>Chen, Shaoying</au><au>Chen, Weibin</au><au>Wu, Jundong</au><au>Gu, Wei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SNHG15 Mediates MTSS1 Gene Expression via Interacting with the Gene Promoter and Regulating Transcription Pausing</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2024-11-01</date><risdate>2024</risdate><volume>25</volume><issue>21</issue><spage>11565</spage><pages>11565-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Metastasis suppressor 1 (MTSS1) has been reported to play important roles in suppressing cancer progression. In this study, we investigated the underlying mechanism that regulates MTSS1 expression. We showed that in breast cancer cells, lncRNA-SNHG15-induced cell invasion and proliferation was accompanied with the decreased expression of MTSS1 mRNA. Further study revealed that SNHG15 mediated MTSS1 repression through blocking its promoter activity. Mechanistically, SNHG15 complexes with DDX5 and RTF1 and interacts with the core promoter of the MTSS1 gene to interfere with RNA-Pol-II-directed transcriptional initiation. Association with DDX5 stabilizes SNHG15 while binding to RTF1 allows SNHG15 to carry RTF1 to the core promoter, where RTF1 forms a complex with PNA pl II to enhance transcriptional pausing. Our findings revealed a molecular mechanism by which SNHG15 serves as a regulator to suppresses MTSS1 transcription via interaction with the gene core promoter.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>39519115</pmid><doi>10.3390/ijms252111565</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Cell growth Cell Line, Tumor Cell Proliferation - genetics DEAD-box RNA Helicases - genetics DEAD-box RNA Helicases - metabolism Development and progression DNA methylation Ethylenediaminetetraacetic acid Female Gene expression Gene Expression Regulation, Neoplastic Genes Genetic aspects Genetic transcription Humans Mediation Messenger RNA Metastasis Microfilament Proteins - genetics Microfilament Proteins - metabolism Neoplasm Proteins - genetics Neoplasm Proteins - metabolism Promoter Regions, Genetic Promoters (Genetics) Proteins RNA polymerase RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Scientific imaging Transcription, Genetic Tumors |
| title | SNHG15 Mediates MTSS1 Gene Expression via Interacting with the Gene Promoter and Regulating Transcription Pausing |
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