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
Hauptverfasser: Wang, Jian, Zhao, Xiangzhai, Guo, Zhaojun, Ma, Xiaolin, Song, Yueqing, Guo, Ying
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container_end_page 1475
container_issue 6
container_start_page 1469
container_title Archives of gynecology and obstetrics
container_volume 295
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
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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 &amp; 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 &amp; 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 &amp; 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 &amp; 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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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