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miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related endometrial cancer
Obesity is a high‐risk factor in the development of endometrial cancer (EC). Our previous study observed that miR‐548ag was significantly overexpressed in the sera of obese individuals. Here, we report the function of miR‐548ag and its mechanism in promoting the obesity‐related progression of EC. Th...
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| Published in: | Cancer science 2023-04, Vol.114 (4), p.1507-1518 |
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| creator | Pang, Huai Wang, Jingzhou Wei, Qianqian Liu, Jie Chu, Xiaolong Yuan, Chenggang Yang, Bingqi Li, Menghuan Ma, Dingling Tang, Yihan Wang, Cuizhe Zhang, Jun |
| description | Obesity is a high‐risk factor in the development of endometrial cancer (EC). Our previous study observed that miR‐548ag was significantly overexpressed in the sera of obese individuals. Here, we report the function of miR‐548ag and its mechanism in promoting the obesity‐related progression of EC. The content of miR‐548ag was increased in the serum of obese EC individuals. Bioinformatics analysis indicated that the survival rate of EC patients with a higher expression of miR‐548ag was significantly reduced. The Mps One Binder Kinase Activator 1B (MOB1B, the core member of the Hippo signaling pathway) is a direct target gene of miR‐548ag, which is inversely correlated with the expression of miR‐548ag. The overexpression of miR‐548ag enhances the proliferation, invasion, and migration, and inhibits apoptosis by downregulating the expression of MOB1B, leading to the deactivation of the Hippo pathway in EC cell lines and contributing to tumor progression in vivo. Our study has established that miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related EC.
Our results indicate that miR‐548ag is a promising diagnostic biomarker to understand the role of the MOB1B/YAP1/CCND1/XIAP axis in promoting obesity‐related EC progression. Starting from clinical issues, this study clarified the molecular mechanism of high expression miR‐548ag in the occurrence and development of obesity‐related EC through in vitro and in vivo experiments, which will provide a theoretical basis for the prevention and treatment of EC. |
| doi_str_mv | 10.1111/cas.15679 |
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Our results indicate that miR‐548ag is a promising diagnostic biomarker to understand the role of the MOB1B/YAP1/CCND1/XIAP axis in promoting obesity‐related EC progression. Starting from clinical issues, this study clarified the molecular mechanism of high expression miR‐548ag in the occurrence and development of obesity‐related EC through in vitro and in vivo experiments, which will provide a theoretical basis for the prevention and treatment of EC.</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/cas.15679</identifier><identifier>PMID: 36445107</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Apoptosis ; Bioinformatics ; Body fat ; Cell culture ; Cell growth ; Cell Line, Tumor ; Cell Movement - genetics ; Cell Proliferation - genetics ; Deactivation ; Endometrial cancer ; Endometrial Neoplasms - metabolism ; Endometrium ; Female ; Gene Expression Regulation, Neoplastic ; Hippo pathway ; Hospitals ; Humans ; Kinases ; Membranes ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miR‐548ag ; MOB1B ; Monoclonal antibodies ; Obesity ; Obesity - complications ; Obesity - genetics ; Oncogenes ; Oncogenes - genetics ; Original ; ORIGINAL ARTICLES ; Polyclonal antibodies ; Reagents ; Risk factors ; Signal transduction ; Tumor cell lines ; Womens health</subject><ispartof>Cancer science, 2023-04, Vol.114 (4), p.1507-1518</ispartof><rights>2022 The Authors. published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2022 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association.</rights><rights>2023. 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-c4689-58d988657457fc0c4199cf4cff2a704f5e2a8b1a4e26b7a4e487bd5cfb0c56d33</citedby><cites>FETCH-LOGICAL-c4689-58d988657457fc0c4199cf4cff2a704f5e2a8b1a4e26b7a4e487bd5cfb0c56d33</cites><orcidid>0000-0001-9796-994X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2793789947/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2793789947?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,315,730,783,787,888,11574,25765,27936,27937,37024,37025,44602,46064,46488,53804,53806,75460</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36445107$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pang, Huai</creatorcontrib><creatorcontrib>Wang, Jingzhou</creatorcontrib><creatorcontrib>Wei, Qianqian</creatorcontrib><creatorcontrib>Liu, Jie</creatorcontrib><creatorcontrib>Chu, Xiaolong</creatorcontrib><creatorcontrib>Yuan, Chenggang</creatorcontrib><creatorcontrib>Yang, Bingqi</creatorcontrib><creatorcontrib>Li, Menghuan</creatorcontrib><creatorcontrib>Ma, Dingling</creatorcontrib><creatorcontrib>Tang, Yihan</creatorcontrib><creatorcontrib>Wang, Cuizhe</creatorcontrib><creatorcontrib>Zhang, Jun</creatorcontrib><title>miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related endometrial cancer</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>Obesity is a high‐risk factor in the development of endometrial cancer (EC). Our previous study observed that miR‐548ag was significantly overexpressed in the sera of obese individuals. Here, we report the function of miR‐548ag and its mechanism in promoting the obesity‐related progression of EC. The content of miR‐548ag was increased in the serum of obese EC individuals. Bioinformatics analysis indicated that the survival rate of EC patients with a higher expression of miR‐548ag was significantly reduced. The Mps One Binder Kinase Activator 1B (MOB1B, the core member of the Hippo signaling pathway) is a direct target gene of miR‐548ag, which is inversely correlated with the expression of miR‐548ag. The overexpression of miR‐548ag enhances the proliferation, invasion, and migration, and inhibits apoptosis by downregulating the expression of MOB1B, leading to the deactivation of the Hippo pathway in EC cell lines and contributing to tumor progression in vivo. Our study has established that miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related EC.
Our results indicate that miR‐548ag is a promising diagnostic biomarker to understand the role of the MOB1B/YAP1/CCND1/XIAP axis in promoting obesity‐related EC progression. Starting from clinical issues, this study clarified the molecular mechanism of high expression miR‐548ag in the occurrence and development of obesity‐related EC through in vitro and in vivo experiments, which will provide a theoretical basis for the prevention and treatment of EC.</description><subject>Apoptosis</subject><subject>Bioinformatics</subject><subject>Body fat</subject><subject>Cell culture</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>Deactivation</subject><subject>Endometrial cancer</subject><subject>Endometrial Neoplasms - metabolism</subject><subject>Endometrium</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Hippo pathway</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Kinases</subject><subject>Membranes</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miR‐548ag</subject><subject>MOB1B</subject><subject>Monoclonal antibodies</subject><subject>Obesity</subject><subject>Obesity - complications</subject><subject>Obesity - genetics</subject><subject>Oncogenes</subject><subject>Oncogenes - genetics</subject><subject>Original</subject><subject>ORIGINAL ARTICLES</subject><subject>Polyclonal antibodies</subject><subject>Reagents</subject><subject>Risk factors</subject><subject>Signal transduction</subject><subject>Tumor cell lines</subject><subject>Womens health</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>PIMPY</sourceid><recordid>eNp1kcFKHTEUhkNpqfa2C1-gBLppF6PJTDKZrEQvVgsWodp1yGROrpGZZJrMWO7OR-gz9kkavSoqNAROIB8ff_IjtEPJLs1rz-i0S3kt5Cu0TSsmC0FI_fruLApJqnILvUvpipCqZpK9RVt5Mk6J2EbT4H78vfnDWaNX2M7eTC74hHXeHgdvwgo84HaN0zyOEVJyfoW_nx3SQ-w8ni4Bd3ANfRgH8BMOFocWkpvW2Rmh1xN0GHwXBpii0z022huI79Ebq_sEH-7nAv38enSxPClOz46_LQ9OC8PqRha86WTT1FwwLqwhhlEpjWXG2lILwiyHUjct1QzKuhV5sEa0HTe2JYbXXVUt0P7GO87tAJ3JEaPu1RjdoONaBe3U8xvvLtUqXCua_09U8tbw-d4Qw68Z0qQGlwz0vfYQ5qRKwcqac5nZBfr0Ar0Kc_T5fZmSlWikZCJTXzaUiSGlCPYxDSXqtkyVy1R3ZWb249P4j-RDexnY2wC_XQ_r_5vU8uB8o_wH3LusNg</recordid><startdate>202304</startdate><enddate>202304</enddate><creator>Pang, Huai</creator><creator>Wang, Jingzhou</creator><creator>Wei, Qianqian</creator><creator>Liu, Jie</creator><creator>Chu, Xiaolong</creator><creator>Yuan, Chenggang</creator><creator>Yang, Bingqi</creator><creator>Li, Menghuan</creator><creator>Ma, Dingling</creator><creator>Tang, Yihan</creator><creator>Wang, Cuizhe</creator><creator>Zhang, Jun</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>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>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-9796-994X</orcidid></search><sort><creationdate>202304</creationdate><title>miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related endometrial cancer</title><author>Pang, Huai ; Wang, Jingzhou ; Wei, Qianqian ; Liu, Jie ; Chu, Xiaolong ; Yuan, Chenggang ; Yang, Bingqi ; Li, Menghuan ; Ma, Dingling ; Tang, Yihan ; Wang, Cuizhe ; Zhang, Jun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4689-58d988657457fc0c4199cf4cff2a704f5e2a8b1a4e26b7a4e487bd5cfb0c56d33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Apoptosis</topic><topic>Bioinformatics</topic><topic>Body fat</topic><topic>Cell culture</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - genetics</topic><topic>Cell Proliferation - genetics</topic><topic>Deactivation</topic><topic>Endometrial cancer</topic><topic>Endometrial Neoplasms - metabolism</topic><topic>Endometrium</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Hippo pathway</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Kinases</topic><topic>Membranes</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miR‐548ag</topic><topic>MOB1B</topic><topic>Monoclonal antibodies</topic><topic>Obesity</topic><topic>Obesity - complications</topic><topic>Obesity - genetics</topic><topic>Oncogenes</topic><topic>Oncogenes - genetics</topic><topic>Original</topic><topic>ORIGINAL ARTICLES</topic><topic>Polyclonal antibodies</topic><topic>Reagents</topic><topic>Risk factors</topic><topic>Signal transduction</topic><topic>Tumor cell lines</topic><topic>Womens health</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pang, Huai</creatorcontrib><creatorcontrib>Wang, Jingzhou</creatorcontrib><creatorcontrib>Wei, Qianqian</creatorcontrib><creatorcontrib>Liu, Jie</creatorcontrib><creatorcontrib>Chu, Xiaolong</creatorcontrib><creatorcontrib>Yuan, Chenggang</creatorcontrib><creatorcontrib>Yang, Bingqi</creatorcontrib><creatorcontrib>Li, Menghuan</creatorcontrib><creatorcontrib>Ma, Dingling</creatorcontrib><creatorcontrib>Tang, Yihan</creatorcontrib><creatorcontrib>Wang, Cuizhe</creatorcontrib><creatorcontrib>Zhang, Jun</creatorcontrib><collection>Wiley Online Library</collection><collection>Wiley-Blackwell Backfiles (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)</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</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</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>MEDLINE - Academic</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>Pang, Huai</au><au>Wang, Jingzhou</au><au>Wei, Qianqian</au><au>Liu, Jie</au><au>Chu, Xiaolong</au><au>Yuan, Chenggang</au><au>Yang, Bingqi</au><au>Li, Menghuan</au><au>Ma, Dingling</au><au>Tang, Yihan</au><au>Wang, Cuizhe</au><au>Zhang, Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related endometrial cancer</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2023-04</date><risdate>2023</risdate><volume>114</volume><issue>4</issue><spage>1507</spage><epage>1518</epage><pages>1507-1518</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>Obesity is a high‐risk factor in the development of endometrial cancer (EC). Our previous study observed that miR‐548ag was significantly overexpressed in the sera of obese individuals. Here, we report the function of miR‐548ag and its mechanism in promoting the obesity‐related progression of EC. The content of miR‐548ag was increased in the serum of obese EC individuals. Bioinformatics analysis indicated that the survival rate of EC patients with a higher expression of miR‐548ag was significantly reduced. The Mps One Binder Kinase Activator 1B (MOB1B, the core member of the Hippo signaling pathway) is a direct target gene of miR‐548ag, which is inversely correlated with the expression of miR‐548ag. The overexpression of miR‐548ag enhances the proliferation, invasion, and migration, and inhibits apoptosis by downregulating the expression of MOB1B, leading to the deactivation of the Hippo pathway in EC cell lines and contributing to tumor progression in vivo. Our study has established that miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related EC.
Our results indicate that miR‐548ag is a promising diagnostic biomarker to understand the role of the MOB1B/YAP1/CCND1/XIAP axis in promoting obesity‐related EC progression. Starting from clinical issues, this study clarified the molecular mechanism of high expression miR‐548ag in the occurrence and development of obesity‐related EC through in vitro and in vivo experiments, which will provide a theoretical basis for the prevention and treatment of EC.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>36445107</pmid><doi>10.1111/cas.15679</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0001-9796-994X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Apoptosis Bioinformatics Body fat Cell culture Cell growth Cell Line, Tumor Cell Movement - genetics Cell Proliferation - genetics Deactivation Endometrial cancer Endometrial Neoplasms - metabolism Endometrium Female Gene Expression Regulation, Neoplastic Hippo pathway Hospitals Humans Kinases Membranes MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miR‐548ag MOB1B Monoclonal antibodies Obesity Obesity - complications Obesity - genetics Oncogenes Oncogenes - genetics Original ORIGINAL ARTICLES Polyclonal antibodies Reagents Risk factors Signal transduction Tumor cell lines Womens health |
| title | miR‐548ag functions as an oncogene by suppressing MOB1B in the development of obesity‐related endometrial cancer |
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