Enhanced nuclear localization of YAP1‐2 contributes to EGF‐induced EMT in NSCLC
YAP1, a key mediator of the Hippo pathway, plays an important role in tumorigenesis. Alternative splicing of human YAP1 mRNA results in two major isoforms: YAP1‐1, which contains a single WW domain, and YAP1‐2, which contains two WW domains, respectively. We here investigated the functions and the u...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2022-02, Vol.26 (4), p.1013-1023 |
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| creator | Guo, Qiang Quan, Mei‐Yu Xu, Le Cai, Yaxin Cai, Jue‐Ting Li, Xue Feng, Guifeng Chen, Aiping Yang, Weiwei Dhlamini, Qhaweni Jiang, Tian‐Fang Shen, Chengguo Chen, Chengshui Zhang, Jin‐San |
| description | YAP1, a key mediator of the Hippo pathway, plays an important role in tumorigenesis. Alternative splicing of human YAP1 mRNA results in two major isoforms: YAP1‐1, which contains a single WW domain, and YAP1‐2, which contains two WW domains, respectively. We here investigated the functions and the underlying regulatory mechanisms of the two YAP1 isoforms in the context of EGF‐induced epithelial‐mesenchymal transition (EMT) in non‐small cell lung cancer (NSCLC). Human NSCLC cell lines express both YAP1‐1 and YAP1‐2 isoforms—although when compared to YAP1‐1, YAP1‐2 mRNA levels are higher while its protein expression levels are lower. EGF treatment significantly promoted YAP1 expression as well as EMT process in NSCLCs, whereas EGF‐induced EMT phenotype was significantly alleviated upon YAP1 knockdown. Under normal culture condition, YAP1‐1 stable expression cells exhibited a stronger migration ability than YAP1‐2 expressing cells. However, upon EGF treatment, YAP1‐2 stable cells showed more robust migration than YAP1‐1 expressing cells. The protein stability and nuclear localization of YAP1‐2 were preferentially enhanced with EGF treatment. Moreover, EGF‐induced EMT and YAP1‐2 activity were suppressed by inhibitor of AKT. Our results suggest that YAP1‐2 is the main isoform that is functionally relevant in promoting EGF‐induced EMT and ultimately NSCLC progression. |
| doi_str_mv | 10.1111/jcmm.17150 |
| format | Article |
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Alternative splicing of human YAP1 mRNA results in two major isoforms: YAP1‐1, which contains a single WW domain, and YAP1‐2, which contains two WW domains, respectively. We here investigated the functions and the underlying regulatory mechanisms of the two YAP1 isoforms in the context of EGF‐induced epithelial‐mesenchymal transition (EMT) in non‐small cell lung cancer (NSCLC). Human NSCLC cell lines express both YAP1‐1 and YAP1‐2 isoforms—although when compared to YAP1‐1, YAP1‐2 mRNA levels are higher while its protein expression levels are lower. EGF treatment significantly promoted YAP1 expression as well as EMT process in NSCLCs, whereas EGF‐induced EMT phenotype was significantly alleviated upon YAP1 knockdown. Under normal culture condition, YAP1‐1 stable expression cells exhibited a stronger migration ability than YAP1‐2 expressing cells. However, upon EGF treatment, YAP1‐2 stable cells showed more robust migration than YAP1‐1 expressing cells. The protein stability and nuclear localization of YAP1‐2 were preferentially enhanced with EGF treatment. Moreover, EGF‐induced EMT and YAP1‐2 activity were suppressed by inhibitor of AKT. Our results suggest that YAP1‐2 is the main isoform that is functionally relevant in promoting EGF‐induced EMT and ultimately NSCLC progression.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.17150</identifier><identifier>PMID: 35014181</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Adaptor Proteins, Signal Transducing - genetics ; Adaptor Proteins, Signal Transducing - metabolism ; AKT protein ; AKT signalling ; Alternative splicing ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - metabolism ; Cell adhesion & migration ; Cell culture ; Cell Line, Tumor ; Cell migration ; EGF ; Epidermal growth factor ; Epidermal Growth Factor - metabolism ; Epidermal Growth Factor - pharmacology ; Epithelial-Mesenchymal Transition - genetics ; epithelial‐mesenchymal transition ; Humans ; Isoforms ; Kinases ; Localization ; Lung cancer ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Mesenchyme ; Metastasis ; mRNA ; Mutation ; Non-small cell lung carcinoma ; NSCLC ; Original ; Phenotypes ; Proteins ; Small cell lung carcinoma ; Software ; Statistical analysis ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Tumor cell lines ; Tumorigenesis ; YAP-Signaling Proteins ; YAP1 isoforms ; Yes-associated protein</subject><ispartof>Journal of cellular and molecular medicine, 2022-02, Vol.26 (4), p.1013-1023</ispartof><rights>2022 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2022 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.</rights><rights>2022. 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><citedby>FETCH-LOGICAL-c4480-266b3963b643b07b778957fd44a1cef4f1dc6b03e9e6e61e48413baceed93da03</citedby><cites>FETCH-LOGICAL-c4480-266b3963b643b07b778957fd44a1cef4f1dc6b03e9e6e61e48413baceed93da03</cites><orcidid>0000-0002-4436-9593 ; 0000-0002-4341-0443</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/PMC8831977/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8831977/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35014181$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guo, Qiang</creatorcontrib><creatorcontrib>Quan, Mei‐Yu</creatorcontrib><creatorcontrib>Xu, Le</creatorcontrib><creatorcontrib>Cai, Yaxin</creatorcontrib><creatorcontrib>Cai, Jue‐Ting</creatorcontrib><creatorcontrib>Li, Xue</creatorcontrib><creatorcontrib>Feng, Guifeng</creatorcontrib><creatorcontrib>Chen, Aiping</creatorcontrib><creatorcontrib>Yang, Weiwei</creatorcontrib><creatorcontrib>Dhlamini, Qhaweni</creatorcontrib><creatorcontrib>Jiang, Tian‐Fang</creatorcontrib><creatorcontrib>Shen, Chengguo</creatorcontrib><creatorcontrib>Chen, Chengshui</creatorcontrib><creatorcontrib>Zhang, Jin‐San</creatorcontrib><title>Enhanced nuclear localization of YAP1‐2 contributes to EGF‐induced EMT in NSCLC</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>YAP1, a key mediator of the Hippo pathway, plays an important role in tumorigenesis. Alternative splicing of human YAP1 mRNA results in two major isoforms: YAP1‐1, which contains a single WW domain, and YAP1‐2, which contains two WW domains, respectively. We here investigated the functions and the underlying regulatory mechanisms of the two YAP1 isoforms in the context of EGF‐induced epithelial‐mesenchymal transition (EMT) in non‐small cell lung cancer (NSCLC). Human NSCLC cell lines express both YAP1‐1 and YAP1‐2 isoforms—although when compared to YAP1‐1, YAP1‐2 mRNA levels are higher while its protein expression levels are lower. EGF treatment significantly promoted YAP1 expression as well as EMT process in NSCLCs, whereas EGF‐induced EMT phenotype was significantly alleviated upon YAP1 knockdown. Under normal culture condition, YAP1‐1 stable expression cells exhibited a stronger migration ability than YAP1‐2 expressing cells. However, upon EGF treatment, YAP1‐2 stable cells showed more robust migration than YAP1‐1 expressing cells. The protein stability and nuclear localization of YAP1‐2 were preferentially enhanced with EGF treatment. Moreover, EGF‐induced EMT and YAP1‐2 activity were suppressed by inhibitor of AKT. Our results suggest that YAP1‐2 is the main isoform that is functionally relevant in promoting EGF‐induced EMT and ultimately NSCLC progression.</description><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>AKT protein</subject><subject>AKT signalling</subject><subject>Alternative splicing</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - metabolism</subject><subject>Cell adhesion & migration</subject><subject>Cell culture</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>EGF</subject><subject>Epidermal growth factor</subject><subject>Epidermal Growth Factor - metabolism</subject><subject>Epidermal Growth Factor - pharmacology</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>epithelial‐mesenchymal transition</subject><subject>Humans</subject><subject>Isoforms</subject><subject>Kinases</subject><subject>Localization</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Mesenchyme</subject><subject>Metastasis</subject><subject>mRNA</subject><subject>Mutation</subject><subject>Non-small cell lung carcinoma</subject><subject>NSCLC</subject><subject>Original</subject><subject>Phenotypes</subject><subject>Proteins</subject><subject>Small cell lung carcinoma</subject><subject>Software</subject><subject>Statistical analysis</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Tumor cell lines</subject><subject>Tumorigenesis</subject><subject>YAP-Signaling Proteins</subject><subject>YAP1 isoforms</subject><subject>Yes-associated protein</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><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>eNp9kUFrFDEYhoMotlYv_gAJeBFha75JNpNchDJsW2VXhdaDp5DJfGOzzCTtZEapJ3-Cv7G_xGx3W9SDuSR8efLwhpeQ58AOIa83a9f3h1DCnD0g-zBXxUxoLh7uzqC42iNPUlozxiVw_Zjs8TkDAQr2ydkiXNjgsKFhch3agXbR2c7_sKOPgcaWfjn6BDc_fxXUxTAOvp5GTHSMdHFynMc-NNPm9WJ1Tn2gH86qZfWUPGptl_DZbj8gn48X59XpbPnx5F11tJw5IRSbFVLWXEteS8FrVtZlqfS8bBshLDhsRQuNkzXjqFGiBBRKAK-tQ2w0byzjB-Tt1ns51T02DnM-25nLwfd2uDbRevP3TfAX5mv8ZpTioMsyC17tBEO8mjCNpvfJYdfZgHFKppCgNBNcb9CX_6DrOA0hfy9TRcmByUJk6vWWckNMacD2Pgwws-nKbLoyt11l-MWf8e_Ru3IyAFvgu-_w-j8q875arbbS3xOtn4E</recordid><startdate>202202</startdate><enddate>202202</enddate><creator>Guo, Qiang</creator><creator>Quan, Mei‐Yu</creator><creator>Xu, Le</creator><creator>Cai, Yaxin</creator><creator>Cai, Jue‐Ting</creator><creator>Li, Xue</creator><creator>Feng, Guifeng</creator><creator>Chen, Aiping</creator><creator>Yang, Weiwei</creator><creator>Dhlamini, Qhaweni</creator><creator>Jiang, Tian‐Fang</creator><creator>Shen, Chengguo</creator><creator>Chen, Chengshui</creator><creator>Zhang, Jin‐San</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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/0000-0002-4436-9593</orcidid><orcidid>https://orcid.org/0000-0002-4341-0443</orcidid></search><sort><creationdate>202202</creationdate><title>Enhanced nuclear localization of YAP1‐2 contributes to EGF‐induced EMT in NSCLC</title><author>Guo, Qiang ; Quan, Mei‐Yu ; Xu, Le ; Cai, Yaxin ; Cai, Jue‐Ting ; Li, Xue ; Feng, Guifeng ; Chen, Aiping ; Yang, Weiwei ; Dhlamini, Qhaweni ; Jiang, Tian‐Fang ; Shen, Chengguo ; Chen, Chengshui ; Zhang, Jin‐San</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4480-266b3963b643b07b778957fd44a1cef4f1dc6b03e9e6e61e48413baceed93da03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>AKT protein</topic><topic>AKT signalling</topic><topic>Alternative splicing</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - metabolism</topic><topic>Cell adhesion & migration</topic><topic>Cell culture</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>EGF</topic><topic>Epidermal growth factor</topic><topic>Epidermal Growth Factor - metabolism</topic><topic>Epidermal Growth Factor - pharmacology</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>epithelial‐mesenchymal transition</topic><topic>Humans</topic><topic>Isoforms</topic><topic>Kinases</topic><topic>Localization</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Mesenchyme</topic><topic>Metastasis</topic><topic>mRNA</topic><topic>Mutation</topic><topic>Non-small cell lung carcinoma</topic><topic>NSCLC</topic><topic>Original</topic><topic>Phenotypes</topic><topic>Proteins</topic><topic>Small cell lung carcinoma</topic><topic>Software</topic><topic>Statistical analysis</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Tumor cell lines</topic><topic>Tumorigenesis</topic><topic>YAP-Signaling Proteins</topic><topic>YAP1 isoforms</topic><topic>Yes-associated protein</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guo, Qiang</creatorcontrib><creatorcontrib>Quan, Mei‐Yu</creatorcontrib><creatorcontrib>Xu, Le</creatorcontrib><creatorcontrib>Cai, Yaxin</creatorcontrib><creatorcontrib>Cai, Jue‐Ting</creatorcontrib><creatorcontrib>Li, Xue</creatorcontrib><creatorcontrib>Feng, Guifeng</creatorcontrib><creatorcontrib>Chen, Aiping</creatorcontrib><creatorcontrib>Yang, Weiwei</creatorcontrib><creatorcontrib>Dhlamini, Qhaweni</creatorcontrib><creatorcontrib>Jiang, Tian‐Fang</creatorcontrib><creatorcontrib>Shen, Chengguo</creatorcontrib><creatorcontrib>Chen, Chengshui</creatorcontrib><creatorcontrib>Zhang, Jin‐San</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library Free Content</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>Guo, Qiang</au><au>Quan, Mei‐Yu</au><au>Xu, Le</au><au>Cai, Yaxin</au><au>Cai, Jue‐Ting</au><au>Li, Xue</au><au>Feng, Guifeng</au><au>Chen, Aiping</au><au>Yang, Weiwei</au><au>Dhlamini, Qhaweni</au><au>Jiang, Tian‐Fang</au><au>Shen, Chengguo</au><au>Chen, Chengshui</au><au>Zhang, Jin‐San</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Enhanced nuclear localization of YAP1‐2 contributes to EGF‐induced EMT in NSCLC</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2022-02</date><risdate>2022</risdate><volume>26</volume><issue>4</issue><spage>1013</spage><epage>1023</epage><pages>1013-1023</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>YAP1, a key mediator of the Hippo pathway, plays an important role in tumorigenesis. Alternative splicing of human YAP1 mRNA results in two major isoforms: YAP1‐1, which contains a single WW domain, and YAP1‐2, which contains two WW domains, respectively. We here investigated the functions and the underlying regulatory mechanisms of the two YAP1 isoforms in the context of EGF‐induced epithelial‐mesenchymal transition (EMT) in non‐small cell lung cancer (NSCLC). Human NSCLC cell lines express both YAP1‐1 and YAP1‐2 isoforms—although when compared to YAP1‐1, YAP1‐2 mRNA levels are higher while its protein expression levels are lower. EGF treatment significantly promoted YAP1 expression as well as EMT process in NSCLCs, whereas EGF‐induced EMT phenotype was significantly alleviated upon YAP1 knockdown. Under normal culture condition, YAP1‐1 stable expression cells exhibited a stronger migration ability than YAP1‐2 expressing cells. However, upon EGF treatment, YAP1‐2 stable cells showed more robust migration than YAP1‐1 expressing cells. The protein stability and nuclear localization of YAP1‐2 were preferentially enhanced with EGF treatment. Moreover, EGF‐induced EMT and YAP1‐2 activity were suppressed by inhibitor of AKT. Our results suggest that YAP1‐2 is the main isoform that is functionally relevant in promoting EGF‐induced EMT and ultimately NSCLC progression.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>35014181</pmid><doi>10.1111/jcmm.17150</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-4436-9593</orcidid><orcidid>https://orcid.org/0000-0002-4341-0443</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of cellular and molecular medicine, 2022-02, Vol.26 (4), p.1013-1023 |
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| source | MEDLINE; Wiley Journals; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); PubMed Central |
| subjects | Adaptor Proteins, Signal Transducing - genetics Adaptor Proteins, Signal Transducing - metabolism AKT protein AKT signalling Alternative splicing Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - metabolism Cell adhesion & migration Cell culture Cell Line, Tumor Cell migration EGF Epidermal growth factor Epidermal Growth Factor - metabolism Epidermal Growth Factor - pharmacology Epithelial-Mesenchymal Transition - genetics epithelial‐mesenchymal transition Humans Isoforms Kinases Localization Lung cancer Lung Neoplasms - genetics Lung Neoplasms - metabolism Mesenchyme Metastasis mRNA Mutation Non-small cell lung carcinoma NSCLC Original Phenotypes Proteins Small cell lung carcinoma Software Statistical analysis Transcription Factors - genetics Transcription Factors - metabolism Tumor cell lines Tumorigenesis YAP-Signaling Proteins YAP1 isoforms Yes-associated protein |
| title | Enhanced nuclear localization of YAP1‐2 contributes to EGF‐induced EMT in NSCLC |
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