RBM4 modulates the proliferation and expression of inflammatory factors via the alternative splicing of regulatory factors in HeLa cells
Regulatory factors function by modulating a variety of cascade mechanisms in cells. RBM4 is a multifunctional RNA-binding protein in post-transcriptional gene regulation. Cytoplasmic RBM4 interacts with Ago2 to regulate inflammatory responses by affecting mRNA decay and cap-dependent translation. Ho...
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| description | Regulatory factors function by modulating a variety of cascade mechanisms in cells. RBM4 is a multifunctional RNA-binding protein in post-transcriptional gene regulation. Cytoplasmic RBM4 interacts with Ago2 to regulate inflammatory responses by affecting mRNA decay and cap-dependent translation. However, it is unclear whether RBM4 functions in inflammation regulation by its splicing factor role. Here, the cell biology, gene expression profile and alternative splicing pattern of HeLa cells with RBM4 overexpression (RBM-OE) were compared with the control. The results showed that RBM4-OE inhibited proliferation. RBM4-OE extensively affects the transcriptional level of genes involved in cell surface receptor signalling pathway, inflammatory responses and the response to lipopolysaccharide. RBM4 broadly regulated the alternative splicing of hundreds of genes with functions of protein binding, helicase activity, DNA binding and transcription co-activator. RBM4-regulated splicing of these genes plays an important role in apoptotic process and gene transcription regulation. As an example, exon inclusion of TNIP1 mediated by RBM4 affects the expression of its targets in inflammatory pathways. These results indicated that RBM4 can mediate the inflammatory response via splicing regulation, which adds to the understanding of the critical role of RBM4 in cancer complicated by inflammation. In conclusion, this study indicated a mechanism in which the dysregulation of alternative splicing can influence cellular biology and lead to various immune-related diseases. |
| doi_str_mv | 10.1007/s00438-019-01606-3 |
| format | Article |
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RBM4 is a multifunctional RNA-binding protein in post-transcriptional gene regulation. Cytoplasmic RBM4 interacts with Ago2 to regulate inflammatory responses by affecting mRNA decay and cap-dependent translation. However, it is unclear whether RBM4 functions in inflammation regulation by its splicing factor role. Here, the cell biology, gene expression profile and alternative splicing pattern of HeLa cells with RBM4 overexpression (RBM-OE) were compared with the control. The results showed that RBM4-OE inhibited proliferation. RBM4-OE extensively affects the transcriptional level of genes involved in cell surface receptor signalling pathway, inflammatory responses and the response to lipopolysaccharide. RBM4 broadly regulated the alternative splicing of hundreds of genes with functions of protein binding, helicase activity, DNA binding and transcription co-activator. RBM4-regulated splicing of these genes plays an important role in apoptotic process and gene transcription regulation. As an example, exon inclusion of TNIP1 mediated by RBM4 affects the expression of its targets in inflammatory pathways. These results indicated that RBM4 can mediate the inflammatory response via splicing regulation, which adds to the understanding of the critical role of RBM4 in cancer complicated by inflammation. In conclusion, this study indicated a mechanism in which the dysregulation of alternative splicing can influence cellular biology and lead to various immune-related diseases.</description><identifier>ISSN: 1617-4615</identifier><identifier>EISSN: 1617-4623</identifier><identifier>DOI: 10.1007/s00438-019-01606-3</identifier><identifier>PMID: 31489484</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Alternative splicing ; Alternative Splicing - genetics ; Animal Genetics and Genomics ; Apoptosis ; Apoptosis - genetics ; Argonaute 2 protein ; Biochemistry ; Biomedical and Life Sciences ; Cell Line, Tumor ; Cell Proliferation - genetics ; Cell surface ; DNA helicase ; DNA-Binding Proteins - genetics ; Exons - genetics ; Gene expression ; Gene regulation ; HeLa Cells ; Human Genetics ; Humans ; Inflammation ; Inflammation - genetics ; Life Sciences ; Lipopolysaccharides ; Microbial Genetics and Genomics ; mRNA turnover ; Original Article ; Plant Genetics and Genomics ; Post-transcription ; RNA Splicing - genetics ; RNA, Messenger - genetics ; RNA-binding protein ; RNA-Binding Proteins - genetics ; Signal transduction ; Signal Transduction - genetics ; Splicing factors ; Transcription Factors - genetics ; Transcription, Genetic - genetics ; Transcriptional Activation - genetics ; Transcriptome - genetics</subject><ispartof>Molecular genetics and genomics : MGG, 2020, Vol.295 (1), p.95-106</ispartof><rights>Springer-Verlag GmbH Germany, part of Springer Nature 2019</rights><rights>Molecular Genetics and Genomics is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-d53907028e76b055306f23eb60c2e65ca36abe93c9682b02cf708f9c7a6be7d93</citedby><cites>FETCH-LOGICAL-c375t-d53907028e76b055306f23eb60c2e65ca36abe93c9682b02cf708f9c7a6be7d93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00438-019-01606-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00438-019-01606-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31489484$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Wei-Yang</creatorcontrib><creatorcontrib>Quan, Weili</creatorcontrib><creatorcontrib>Yang, Fan</creatorcontrib><creatorcontrib>Wei, Ya-Xun</creatorcontrib><creatorcontrib>Chen, Jia-Jun</creatorcontrib><creatorcontrib>Yu, Han</creatorcontrib><creatorcontrib>Xie, Jie</creatorcontrib><creatorcontrib>Zhang, Yi</creatorcontrib><creatorcontrib>Li, Zhan-Fei</creatorcontrib><title>RBM4 modulates the proliferation and expression of inflammatory factors via the alternative splicing of regulatory factors in HeLa cells</title><title>Molecular genetics and genomics : MGG</title><addtitle>Mol Genet Genomics</addtitle><addtitle>Mol Genet Genomics</addtitle><description>Regulatory factors function by modulating a variety of cascade mechanisms in cells. RBM4 is a multifunctional RNA-binding protein in post-transcriptional gene regulation. Cytoplasmic RBM4 interacts with Ago2 to regulate inflammatory responses by affecting mRNA decay and cap-dependent translation. However, it is unclear whether RBM4 functions in inflammation regulation by its splicing factor role. Here, the cell biology, gene expression profile and alternative splicing pattern of HeLa cells with RBM4 overexpression (RBM-OE) were compared with the control. The results showed that RBM4-OE inhibited proliferation. RBM4-OE extensively affects the transcriptional level of genes involved in cell surface receptor signalling pathway, inflammatory responses and the response to lipopolysaccharide. RBM4 broadly regulated the alternative splicing of hundreds of genes with functions of protein binding, helicase activity, DNA binding and transcription co-activator. RBM4-regulated splicing of these genes plays an important role in apoptotic process and gene transcription regulation. As an example, exon inclusion of TNIP1 mediated by RBM4 affects the expression of its targets in inflammatory pathways. These results indicated that RBM4 can mediate the inflammatory response via splicing regulation, which adds to the understanding of the critical role of RBM4 in cancer complicated by inflammation. In conclusion, this study indicated a mechanism in which the dysregulation of alternative splicing can influence cellular biology and lead to various immune-related diseases.</description><subject>Alternative splicing</subject><subject>Alternative Splicing - genetics</subject><subject>Animal Genetics and Genomics</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Argonaute 2 protein</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - genetics</subject><subject>Cell surface</subject><subject>DNA helicase</subject><subject>DNA-Binding Proteins - genetics</subject><subject>Exons - genetics</subject><subject>Gene expression</subject><subject>Gene regulation</subject><subject>HeLa Cells</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - genetics</subject><subject>Life Sciences</subject><subject>Lipopolysaccharides</subject><subject>Microbial Genetics and Genomics</subject><subject>mRNA turnover</subject><subject>Original Article</subject><subject>Plant Genetics and Genomics</subject><subject>Post-transcription</subject><subject>RNA Splicing - genetics</subject><subject>RNA, Messenger - genetics</subject><subject>RNA-binding protein</subject><subject>RNA-Binding Proteins - genetics</subject><subject>Signal transduction</subject><subject>Signal Transduction - genetics</subject><subject>Splicing factors</subject><subject>Transcription Factors - genetics</subject><subject>Transcription, Genetic - genetics</subject><subject>Transcriptional Activation - genetics</subject><subject>Transcriptome - genetics</subject><issn>1617-4615</issn><issn>1617-4623</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc1O3DAUhS3UqlDoC7BAlrrpJuCfxD_LFrUFaVClqqwtx7kejJxksBNU3qCPjTMDtGLRhXVt-Tvn-vogdEzJKSVEnmVCaq4qQnVZgoiK76EDKqisasH4m5c9bfbR-5xvCaFSMPkO7XNaK12r-gD9-fnlqsb92M3RTpDxdAN4k8YYPCQ7hXHAdugw_N4kyHk5jh6HwUfb93Ya0wP21pWa8X2wW7GNE6ShSO8B500MLgzrRZRgvbT4VxIGfAErix3EmI_QW29jhg9P9RBdf_v66_yiWv34fnn-eVU5Lpup6hquiSRMgRQtaRpOhGccWkEcA9E4y4VtQXOnhWItYc5Lorx20ooWZKf5Ifq08y1T3s2QJ9OHvLzADjDO2TCmhK7L_9KCfnyF3o5zmS1uqVo1VGlVKLajXBpzTuDNJoXepgdDiVlyMrucTMnJbHMyvIhOnqzntofuRfIcTAH4DsjlalhD-tv7P7aP8d-fXA</recordid><startdate>2020</startdate><enddate>2020</enddate><creator>Wang, Wei-Yang</creator><creator>Quan, Weili</creator><creator>Yang, Fan</creator><creator>Wei, Ya-Xun</creator><creator>Chen, Jia-Jun</creator><creator>Yu, Han</creator><creator>Xie, Jie</creator><creator>Zhang, Yi</creator><creator>Li, Zhan-Fei</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</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>7SS</scope><scope>7TK</scope><scope>7TM</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</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>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>2020</creationdate><title>RBM4 modulates the proliferation and expression of inflammatory factors via the alternative splicing of regulatory factors in HeLa cells</title><author>Wang, Wei-Yang ; Quan, Weili ; Yang, Fan ; Wei, Ya-Xun ; Chen, Jia-Jun ; Yu, Han ; Xie, Jie ; Zhang, Yi ; Li, Zhan-Fei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-d53907028e76b055306f23eb60c2e65ca36abe93c9682b02cf708f9c7a6be7d93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Alternative splicing</topic><topic>Alternative Splicing - genetics</topic><topic>Animal Genetics and Genomics</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Argonaute 2 protein</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - genetics</topic><topic>Cell surface</topic><topic>DNA helicase</topic><topic>DNA-Binding Proteins - genetics</topic><topic>Exons - genetics</topic><topic>Gene expression</topic><topic>Gene regulation</topic><topic>HeLa Cells</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammation - genetics</topic><topic>Life Sciences</topic><topic>Lipopolysaccharides</topic><topic>Microbial Genetics and Genomics</topic><topic>mRNA turnover</topic><topic>Original Article</topic><topic>Plant Genetics and Genomics</topic><topic>Post-transcription</topic><topic>RNA Splicing - genetics</topic><topic>RNA, Messenger - genetics</topic><topic>RNA-binding protein</topic><topic>RNA-Binding Proteins - genetics</topic><topic>Signal transduction</topic><topic>Signal Transduction - genetics</topic><topic>Splicing factors</topic><topic>Transcription Factors - genetics</topic><topic>Transcription, Genetic - genetics</topic><topic>Transcriptional Activation - genetics</topic><topic>Transcriptome - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Wei-Yang</creatorcontrib><creatorcontrib>Quan, Weili</creatorcontrib><creatorcontrib>Yang, Fan</creatorcontrib><creatorcontrib>Wei, Ya-Xun</creatorcontrib><creatorcontrib>Chen, Jia-Jun</creatorcontrib><creatorcontrib>Yu, Han</creatorcontrib><creatorcontrib>Xie, Jie</creatorcontrib><creatorcontrib>Zhang, Yi</creatorcontrib><creatorcontrib>Li, Zhan-Fei</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>Entomology Abstracts (Full archive)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical 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>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular genetics and genomics : MGG</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Wei-Yang</au><au>Quan, Weili</au><au>Yang, Fan</au><au>Wei, Ya-Xun</au><au>Chen, Jia-Jun</au><au>Yu, Han</au><au>Xie, Jie</au><au>Zhang, Yi</au><au>Li, Zhan-Fei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>RBM4 modulates the proliferation and expression of inflammatory factors via the alternative splicing of regulatory factors in HeLa cells</atitle><jtitle>Molecular genetics and genomics : MGG</jtitle><stitle>Mol Genet Genomics</stitle><addtitle>Mol Genet Genomics</addtitle><date>2020</date><risdate>2020</risdate><volume>295</volume><issue>1</issue><spage>95</spage><epage>106</epage><pages>95-106</pages><issn>1617-4615</issn><eissn>1617-4623</eissn><abstract>Regulatory factors function by modulating a variety of cascade mechanisms in cells. RBM4 is a multifunctional RNA-binding protein in post-transcriptional gene regulation. Cytoplasmic RBM4 interacts with Ago2 to regulate inflammatory responses by affecting mRNA decay and cap-dependent translation. However, it is unclear whether RBM4 functions in inflammation regulation by its splicing factor role. Here, the cell biology, gene expression profile and alternative splicing pattern of HeLa cells with RBM4 overexpression (RBM-OE) were compared with the control. The results showed that RBM4-OE inhibited proliferation. RBM4-OE extensively affects the transcriptional level of genes involved in cell surface receptor signalling pathway, inflammatory responses and the response to lipopolysaccharide. RBM4 broadly regulated the alternative splicing of hundreds of genes with functions of protein binding, helicase activity, DNA binding and transcription co-activator. RBM4-regulated splicing of these genes plays an important role in apoptotic process and gene transcription regulation. As an example, exon inclusion of TNIP1 mediated by RBM4 affects the expression of its targets in inflammatory pathways. These results indicated that RBM4 can mediate the inflammatory response via splicing regulation, which adds to the understanding of the critical role of RBM4 in cancer complicated by inflammation. In conclusion, this study indicated a mechanism in which the dysregulation of alternative splicing can influence cellular biology and lead to various immune-related diseases.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>31489484</pmid><doi>10.1007/s00438-019-01606-3</doi><tpages>12</tpages></addata></record> |
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| subjects | Alternative splicing Alternative Splicing - genetics Animal Genetics and Genomics Apoptosis Apoptosis - genetics Argonaute 2 protein Biochemistry Biomedical and Life Sciences Cell Line, Tumor Cell Proliferation - genetics Cell surface DNA helicase DNA-Binding Proteins - genetics Exons - genetics Gene expression Gene regulation HeLa Cells Human Genetics Humans Inflammation Inflammation - genetics Life Sciences Lipopolysaccharides Microbial Genetics and Genomics mRNA turnover Original Article Plant Genetics and Genomics Post-transcription RNA Splicing - genetics RNA, Messenger - genetics RNA-binding protein RNA-Binding Proteins - genetics Signal transduction Signal Transduction - genetics Splicing factors Transcription Factors - genetics Transcription, Genetic - genetics Transcriptional Activation - genetics Transcriptome - genetics |
| title | RBM4 modulates the proliferation and expression of inflammatory factors via the alternative splicing of regulatory factors in HeLa cells |
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