Regulation of NEAT1/miR-214-3p on the growth, migration and invasion of endometrial carcinoma cells
Objective To investigate the function and mechanism of lnc NEAT1 in regulating the growth, migration and invasion of endometrial carcinoma (EC) cells. Materials and methods NEAT1 and miR-214-3p levels were measured by qRT-PCR. The protein levels of HMGA1, β-catenin, c-myc and MMP9 were evaluated by...
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Veröffentlicht in: | Archives of gynecology and obstetrics 2017-06, Vol.295 (6), p.1469-1475 |
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creator | Wang, Jian Zhao, Xiangzhai Guo, Zhaojun Ma, Xiaolin Song, Yueqing Guo, Ying |
description | Objective
To investigate the function and mechanism of lnc NEAT1 in regulating the growth, migration and invasion of endometrial carcinoma (EC) cells.
Materials and methods
NEAT1 and miR-214-3p levels were measured by qRT-PCR. The protein levels of HMGA1, β-catenin, c-myc and MMP9 were evaluated by Western blot. The effects of NEAT1, HMGA1, miR-214-3p on the viability, migration and invasion of HEC-1A cells were accessed by WST-1 assay and transwell migration/invasion assay. The effect of miR-214-3p on Wnt signaling activity was tested by luciferase reporter assay.
Results
NEAT1, HMGA1 and β-catenin were significantly upregulated in EC tissues, and miR-214-3p was significantly downregulated. NEAT1 promoted the growth, migration and invasion of HEC-1A cells, and mRNA level of Wnt/β-catenin downstream genes c-myc and MMP9. In addition, HMGA1 upregualted the protein and mRNA levels of Wnt/β-catenin downstream genes c-myc and MMP9, and could improve cell viability, and increase numbers of migration and invasion of HEC-1A cells. miR-214-3p overexpression inhibited the proliferation, migration and invasion of HEC-1A cells, while NEAT1 overexpression reversed these effects. miR-214-3p overexpression inhibited the activity of Wnt/β-catenin pathway, while NEAT1 overexpression reversed this effect. Then, si-HMGA1 reduced the activity of Wnt/β-catenin pathway. Moreover, we found NEAT1 and HMGA1 bound to miR-214-3p by luciferase reporter assay, and NEAT1 and HMGA1 expression were negatively correlated with miR-214-3p.
Conclusion
NEAT1 regulates HMGA1 via miR-214-3p to regulate Wnt/β-catenin pathway, thus promotes the growth, migration and invasion of HEC-1A cells. |
doi_str_mv | 10.1007/s00404-017-4365-1 |
format | Article |
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To investigate the function and mechanism of lnc NEAT1 in regulating the growth, migration and invasion of endometrial carcinoma (EC) cells.
Materials and methods
NEAT1 and miR-214-3p levels were measured by qRT-PCR. The protein levels of HMGA1, β-catenin, c-myc and MMP9 were evaluated by Western blot. The effects of NEAT1, HMGA1, miR-214-3p on the viability, migration and invasion of HEC-1A cells were accessed by WST-1 assay and transwell migration/invasion assay. The effect of miR-214-3p on Wnt signaling activity was tested by luciferase reporter assay.
Results
NEAT1, HMGA1 and β-catenin were significantly upregulated in EC tissues, and miR-214-3p was significantly downregulated. NEAT1 promoted the growth, migration and invasion of HEC-1A cells, and mRNA level of Wnt/β-catenin downstream genes c-myc and MMP9. In addition, HMGA1 upregualted the protein and mRNA levels of Wnt/β-catenin downstream genes c-myc and MMP9, and could improve cell viability, and increase numbers of migration and invasion of HEC-1A cells. miR-214-3p overexpression inhibited the proliferation, migration and invasion of HEC-1A cells, while NEAT1 overexpression reversed these effects. miR-214-3p overexpression inhibited the activity of Wnt/β-catenin pathway, while NEAT1 overexpression reversed this effect. Then, si-HMGA1 reduced the activity of Wnt/β-catenin pathway. Moreover, we found NEAT1 and HMGA1 bound to miR-214-3p by luciferase reporter assay, and NEAT1 and HMGA1 expression were negatively correlated with miR-214-3p.
Conclusion
NEAT1 regulates HMGA1 via miR-214-3p to regulate Wnt/β-catenin pathway, thus promotes the growth, migration and invasion of HEC-1A cells.</description><identifier>ISSN: 0932-0067</identifier><identifier>EISSN: 1432-0711</identifier><identifier>DOI: 10.1007/s00404-017-4365-1</identifier><identifier>PMID: 28447190</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>beta Catenin ; Blotting, Western ; Cell Line, Tumor ; Cell Proliferation ; Endocrinology ; Endometrial cancer ; Endometrial Neoplasms - genetics ; Endometrial Neoplasms - pathology ; Female ; Gene Expression Regulation, Neoplastic ; Gynecologic Oncology ; Gynecology ; Human Genetics ; Humans ; Matrix Metalloproteinase 9 - metabolism ; Medicine ; Medicine & Public Health ; MicroRNAs - metabolism ; MicroRNAs - physiology ; Neoplasm Invasiveness - genetics ; Neoplasm Invasiveness - pathology ; Obstetrics/Perinatology/Midwifery ; Real-Time Polymerase Chain Reaction ; RNA, Long Noncoding - genetics ; RNA, Long Noncoding - metabolism ; Wnt Signaling Pathway</subject><ispartof>Archives of gynecology and obstetrics, 2017-06, Vol.295 (6), p.1469-1475</ispartof><rights>Springer-Verlag Berlin Heidelberg 2017</rights><rights>Archives of Gynecology and Obstetrics is a copyright of Springer, (2017). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-63ef57a70adab70f54de0c8edda92b5f150518e96c1f97075fc534473dec96de3</citedby><cites>FETCH-LOGICAL-c438t-63ef57a70adab70f54de0c8edda92b5f150518e96c1f97075fc534473dec96de3</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/s00404-017-4365-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00404-017-4365-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28447190$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Jian</creatorcontrib><creatorcontrib>Zhao, Xiangzhai</creatorcontrib><creatorcontrib>Guo, Zhaojun</creatorcontrib><creatorcontrib>Ma, Xiaolin</creatorcontrib><creatorcontrib>Song, Yueqing</creatorcontrib><creatorcontrib>Guo, Ying</creatorcontrib><title>Regulation of NEAT1/miR-214-3p on the growth, migration and invasion of endometrial carcinoma cells</title><title>Archives of gynecology and obstetrics</title><addtitle>Arch Gynecol Obstet</addtitle><addtitle>Arch Gynecol Obstet</addtitle><description>Objective
To investigate the function and mechanism of lnc NEAT1 in regulating the growth, migration and invasion of endometrial carcinoma (EC) cells.
Materials and methods
NEAT1 and miR-214-3p levels were measured by qRT-PCR. The protein levels of HMGA1, β-catenin, c-myc and MMP9 were evaluated by Western blot. The effects of NEAT1, HMGA1, miR-214-3p on the viability, migration and invasion of HEC-1A cells were accessed by WST-1 assay and transwell migration/invasion assay. The effect of miR-214-3p on Wnt signaling activity was tested by luciferase reporter assay.
Results
NEAT1, HMGA1 and β-catenin were significantly upregulated in EC tissues, and miR-214-3p was significantly downregulated. NEAT1 promoted the growth, migration and invasion of HEC-1A cells, and mRNA level of Wnt/β-catenin downstream genes c-myc and MMP9. In addition, HMGA1 upregualted the protein and mRNA levels of Wnt/β-catenin downstream genes c-myc and MMP9, and could improve cell viability, and increase numbers of migration and invasion of HEC-1A cells. miR-214-3p overexpression inhibited the proliferation, migration and invasion of HEC-1A cells, while NEAT1 overexpression reversed these effects. miR-214-3p overexpression inhibited the activity of Wnt/β-catenin pathway, while NEAT1 overexpression reversed this effect. Then, si-HMGA1 reduced the activity of Wnt/β-catenin pathway. Moreover, we found NEAT1 and HMGA1 bound to miR-214-3p by luciferase reporter assay, and NEAT1 and HMGA1 expression were negatively correlated with miR-214-3p.
Conclusion
NEAT1 regulates HMGA1 via miR-214-3p to regulate Wnt/β-catenin pathway, thus promotes the growth, migration and invasion of HEC-1A cells.</description><subject>beta Catenin</subject><subject>Blotting, Western</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Endocrinology</subject><subject>Endometrial cancer</subject><subject>Endometrial Neoplasms - genetics</subject><subject>Endometrial Neoplasms - pathology</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gynecologic Oncology</subject><subject>Gynecology</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Matrix Metalloproteinase 9 - metabolism</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>MicroRNAs - metabolism</subject><subject>MicroRNAs - physiology</subject><subject>Neoplasm Invasiveness - genetics</subject><subject>Neoplasm Invasiveness - pathology</subject><subject>Obstetrics/Perinatology/Midwifery</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>RNA, Long Noncoding - genetics</subject><subject>RNA, Long Noncoding - metabolism</subject><subject>Wnt Signaling Pathway</subject><issn>0932-0067</issn><issn>1432-0711</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kV2L1TAQhoMo7nH1B3gjBW-8MO5MPprmclnWD1gUlvU65CTTs13a5pi0iv_elh4VBK8yJM_7zmRexl4ivEMAc1EAFCgOaLiSteb4iO1QScHBID5mO7BrDbU5Y89KeQBA0TT1U3YmGqUMWtixcEuHufdTl8YqtdXn68s7vBi6Wy5QcXmsluvpnqpDTj-m-7fV0B3yBvsxVt343ZeTksaYBppy5_sq-By6MQ2-CtT35Tl70vq-0IvTec6-vr--u_rIb758-HR1ecODks3Ea0mtNt6Aj35voNUqEoSGYvRW7HWLGjQ2ZOuArTVgdBu0XP4hIwVbR5Ln7M3me8zp20xlckNX1gn8SGkuDhsrjJDG2gV9_Q_6kOY8LtM5IWrUQlpcKdyokFMpmVp3zN3g80-H4NYE3JaAWxJwawIOF82rk_O8Hyj-Ufxe-QKIDSjL03ig_Lf1_11_AasYj10</recordid><startdate>20170601</startdate><enddate>20170601</enddate><creator>Wang, Jian</creator><creator>Zhao, Xiangzhai</creator><creator>Guo, Zhaojun</creator><creator>Ma, Xiaolin</creator><creator>Song, Yueqing</creator><creator>Guo, Ying</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>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20170601</creationdate><title>Regulation of NEAT1/miR-214-3p on the growth, migration and invasion of endometrial carcinoma cells</title><author>Wang, Jian ; Zhao, Xiangzhai ; Guo, Zhaojun ; Ma, Xiaolin ; Song, Yueqing ; Guo, Ying</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c438t-63ef57a70adab70f54de0c8edda92b5f150518e96c1f97075fc534473dec96de3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>beta Catenin</topic><topic>Blotting, Western</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Endocrinology</topic><topic>Endometrial cancer</topic><topic>Endometrial Neoplasms - genetics</topic><topic>Endometrial Neoplasms - pathology</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gynecologic Oncology</topic><topic>Gynecology</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Matrix Metalloproteinase 9 - metabolism</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>MicroRNAs - metabolism</topic><topic>MicroRNAs - physiology</topic><topic>Neoplasm Invasiveness - genetics</topic><topic>Neoplasm Invasiveness - pathology</topic><topic>Obstetrics/Perinatology/Midwifery</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>RNA, Long Noncoding - genetics</topic><topic>RNA, Long Noncoding - metabolism</topic><topic>Wnt Signaling Pathway</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Jian</creatorcontrib><creatorcontrib>Zhao, Xiangzhai</creatorcontrib><creatorcontrib>Guo, Zhaojun</creatorcontrib><creatorcontrib>Ma, Xiaolin</creatorcontrib><creatorcontrib>Song, Yueqing</creatorcontrib><creatorcontrib>Guo, Ying</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>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</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</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><jtitle>Archives of gynecology and obstetrics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Jian</au><au>Zhao, Xiangzhai</au><au>Guo, Zhaojun</au><au>Ma, Xiaolin</au><au>Song, Yueqing</au><au>Guo, Ying</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of NEAT1/miR-214-3p on the growth, migration and invasion of endometrial carcinoma cells</atitle><jtitle>Archives of gynecology and obstetrics</jtitle><stitle>Arch Gynecol Obstet</stitle><addtitle>Arch Gynecol Obstet</addtitle><date>2017-06-01</date><risdate>2017</risdate><volume>295</volume><issue>6</issue><spage>1469</spage><epage>1475</epage><pages>1469-1475</pages><issn>0932-0067</issn><eissn>1432-0711</eissn><abstract>Objective
To investigate the function and mechanism of lnc NEAT1 in regulating the growth, migration and invasion of endometrial carcinoma (EC) cells.
Materials and methods
NEAT1 and miR-214-3p levels were measured by qRT-PCR. The protein levels of HMGA1, β-catenin, c-myc and MMP9 were evaluated by Western blot. The effects of NEAT1, HMGA1, miR-214-3p on the viability, migration and invasion of HEC-1A cells were accessed by WST-1 assay and transwell migration/invasion assay. The effect of miR-214-3p on Wnt signaling activity was tested by luciferase reporter assay.
Results
NEAT1, HMGA1 and β-catenin were significantly upregulated in EC tissues, and miR-214-3p was significantly downregulated. NEAT1 promoted the growth, migration and invasion of HEC-1A cells, and mRNA level of Wnt/β-catenin downstream genes c-myc and MMP9. In addition, HMGA1 upregualted the protein and mRNA levels of Wnt/β-catenin downstream genes c-myc and MMP9, and could improve cell viability, and increase numbers of migration and invasion of HEC-1A cells. miR-214-3p overexpression inhibited the proliferation, migration and invasion of HEC-1A cells, while NEAT1 overexpression reversed these effects. miR-214-3p overexpression inhibited the activity of Wnt/β-catenin pathway, while NEAT1 overexpression reversed this effect. Then, si-HMGA1 reduced the activity of Wnt/β-catenin pathway. Moreover, we found NEAT1 and HMGA1 bound to miR-214-3p by luciferase reporter assay, and NEAT1 and HMGA1 expression were negatively correlated with miR-214-3p.
Conclusion
NEAT1 regulates HMGA1 via miR-214-3p to regulate Wnt/β-catenin pathway, thus promotes the growth, migration and invasion of HEC-1A cells.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>28447190</pmid><doi>10.1007/s00404-017-4365-1</doi><tpages>7</tpages></addata></record> |
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subjects | beta Catenin Blotting, Western Cell Line, Tumor Cell Proliferation Endocrinology Endometrial cancer Endometrial Neoplasms - genetics Endometrial Neoplasms - pathology Female Gene Expression Regulation, Neoplastic Gynecologic Oncology Gynecology Human Genetics Humans Matrix Metalloproteinase 9 - metabolism Medicine Medicine & Public Health MicroRNAs - metabolism MicroRNAs - physiology Neoplasm Invasiveness - genetics Neoplasm Invasiveness - pathology Obstetrics/Perinatology/Midwifery Real-Time Polymerase Chain Reaction RNA, Long Noncoding - genetics RNA, Long Noncoding - metabolism Wnt Signaling Pathway |
title | Regulation of NEAT1/miR-214-3p on the growth, migration and invasion of endometrial carcinoma cells |
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