miR-21 regulates growth and EMT in lung cancer cells via PTEN/Akt/GSK3β signaling
miRNA-21 (miR-21) is overexpressed in various human cancers. Here, we show that miR-21 is overexpressed in human Non-Small Cell Lung Cancer (NSCLC) and that its up or down-regulation, respectively, increases or decreases cyclin D1 and cyclin E1 expression and coordinately promotes or inhibits proli...
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Veröffentlicht in: | Frontiers in bioscience 2019-06, Vol.24 (8), p.1426-1439, Article 4788 |
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creator | Dai, Lihua Chen, Fenghua Zheng, Yonghua Zhang, Ding Qian, Bao Ji, Huaxia Long, Feng Cretoiu, Dragos |
description | miRNA-21 (miR-21) is overexpressed in various human cancers. Here, we show that miR-21 is overexpressed in human Non-Small Cell Lung Cancer (NSCLC) and that its up or down-regulation, respectively, increases or decreases cyclin D1 and cyclin E1 expression and coordinately promotes or inhibits proliferation of cancer cells. The perturbations of miR-21 also dramatically reduces or increases epithelial to mesenschymal transition (EMT). We show that regulation of proliferation and EMT are directed by PTEN/Akt/GSK3 beta signaling axis by regulating the expression of invasion markers including E-cadherin, vimentin, snail, slug and beta-catenin. Together, these findings show that miR-21 is a potential target for the development of treatment for NSCLC forms of human lung cancer. |
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Here, we show that miR-21 is overexpressed in human Non-Small Cell Lung Cancer (NSCLC) and that its up or down-regulation, respectively, increases or decreases cyclin D1 and cyclin E1 expression and coordinately promotes or inhibits proliferation of cancer cells. The perturbations of miR-21 also dramatically reduces or increases epithelial to mesenschymal transition (EMT). We show that regulation of proliferation and EMT are directed by PTEN/Akt/GSK3 beta signaling axis by regulating the expression of invasion markers including E-cadherin, vimentin, snail, slug and beta-catenin. Together, these findings show that miR-21 is a potential target for the development of treatment for NSCLC forms of human lung cancer.</description><identifier>ISSN: 1093-9946</identifier><identifier>EISSN: 2768-6698</identifier><identifier>EISSN: 1093-4715</identifier><identifier>DOI: 10.2741/4788</identifier><identifier>PMID: 31136988</identifier><language>eng</language><publisher>Singapore</publisher><subject>A549 Cells ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - metabolism ; Carcinoma, Non-Small-Cell Lung - pathology ; Cell Line, Tumor ; Cell Proliferation - genetics ; Cyclins - genetics ; Cyclins - metabolism ; Epithelial-Mesenchymal Transition - genetics ; Gene Expression Regulation, Neoplastic ; Glycogen Synthase Kinase 3 beta - genetics ; Glycogen Synthase Kinase 3 beta - metabolism ; Humans ; Lung Neoplasms - genetics ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; MicroRNAs - genetics ; Proto-Oncogene Proteins c-akt - genetics ; Proto-Oncogene Proteins c-akt - metabolism ; PTEN Phosphohydrolase - genetics ; PTEN Phosphohydrolase - metabolism ; Signal Transduction - genetics</subject><ispartof>Frontiers in bioscience, 2019-06, Vol.24 (8), p.1426-1439, Article 4788</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c275t-556c48b88382f9d358d745dc1137bb5942c7ad11db6e264cf0c01237934aeefe3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31136988$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dai, Lihua</creatorcontrib><creatorcontrib>Chen, Fenghua</creatorcontrib><creatorcontrib>Zheng, Yonghua</creatorcontrib><creatorcontrib>Zhang, Ding</creatorcontrib><creatorcontrib>Qian, Bao</creatorcontrib><creatorcontrib>Ji, Huaxia</creatorcontrib><creatorcontrib>Long, Feng</creatorcontrib><creatorcontrib>Cretoiu, Dragos</creatorcontrib><title>miR-21 regulates growth and EMT in lung cancer cells via PTEN/Akt/GSK3β signaling</title><title>Frontiers in bioscience</title><addtitle>Front Biosci (Landmark Ed)</addtitle><description>miRNA-21 (miR-21) is overexpressed in various human cancers. Here, we show that miR-21 is overexpressed in human Non-Small Cell Lung Cancer (NSCLC) and that its up or down-regulation, respectively, increases or decreases cyclin D1 and cyclin E1 expression and coordinately promotes or inhibits proliferation of cancer cells. The perturbations of miR-21 also dramatically reduces or increases epithelial to mesenschymal transition (EMT). We show that regulation of proliferation and EMT are directed by PTEN/Akt/GSK3 beta signaling axis by regulating the expression of invasion markers including E-cadherin, vimentin, snail, slug and beta-catenin. Together, these findings show that miR-21 is a potential target for the development of treatment for NSCLC forms of human lung cancer.</description><subject>A549 Cells</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - metabolism</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - genetics</subject><subject>Cyclins - genetics</subject><subject>Cyclins - metabolism</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Glycogen Synthase Kinase 3 beta - genetics</subject><subject>Glycogen Synthase Kinase 3 beta - metabolism</subject><subject>Humans</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>MicroRNAs - genetics</subject><subject>Proto-Oncogene Proteins c-akt - genetics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>PTEN Phosphohydrolase - metabolism</subject><subject>Signal Transduction - genetics</subject><issn>1093-9946</issn><issn>2768-6698</issn><issn>1093-4715</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kMtOwkAARSdGIwT4BTMLF24q834sCUE04iOI62Y6ndZqHzjTavwtP8RvsgR0dTcnNycHgDFGl0QyPGVSqSMwJFKoSAitjsEQI00jrZkYgEkIrwghojHWXJ2CAcWY9pQagnVVrCOCoXd5V5rWBZj75rN9gaZO4eJuA4sall2dQ2tq6zy0riwD_CgMfNws7qezt3a6fLqlP98wFHltyqLOx-AkM2Vwk8OOwPPVYjO_jlYPy5v5bBVZInkbcS4sU4lSVJFMp5SrVDKe2l5NJgnXjFhpUozTRDgimM2QRZhQqSkzzmWOjsDF_nfrm_fOhTauirDzM7VruhATQrHigiDSo-d71PomBO-yeOuLyvivGKN4FzDeBeyxs8Njl1Qu_Yf-ctFfs6tnpw</recordid><startdate>20190601</startdate><enddate>20190601</enddate><creator>Dai, Lihua</creator><creator>Chen, Fenghua</creator><creator>Zheng, Yonghua</creator><creator>Zhang, Ding</creator><creator>Qian, Bao</creator><creator>Ji, Huaxia</creator><creator>Long, Feng</creator><creator>Cretoiu, Dragos</creator><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>7X8</scope></search><sort><creationdate>20190601</creationdate><title>miR-21 regulates growth and EMT in lung cancer cells via PTEN/Akt/GSK3β signaling</title><author>Dai, Lihua ; Chen, Fenghua ; Zheng, Yonghua ; Zhang, Ding ; Qian, Bao ; Ji, Huaxia ; Long, Feng ; Cretoiu, Dragos</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c275t-556c48b88382f9d358d745dc1137bb5942c7ad11db6e264cf0c01237934aeefe3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>A549 Cells</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - metabolism</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - genetics</topic><topic>Cyclins - genetics</topic><topic>Cyclins - metabolism</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Glycogen Synthase Kinase 3 beta - genetics</topic><topic>Glycogen Synthase Kinase 3 beta - metabolism</topic><topic>Humans</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>MicroRNAs - genetics</topic><topic>Proto-Oncogene Proteins c-akt - genetics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>PTEN Phosphohydrolase - metabolism</topic><topic>Signal Transduction - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dai, Lihua</creatorcontrib><creatorcontrib>Chen, Fenghua</creatorcontrib><creatorcontrib>Zheng, Yonghua</creatorcontrib><creatorcontrib>Zhang, Ding</creatorcontrib><creatorcontrib>Qian, Bao</creatorcontrib><creatorcontrib>Ji, Huaxia</creatorcontrib><creatorcontrib>Long, Feng</creatorcontrib><creatorcontrib>Cretoiu, Dragos</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Frontiers in bioscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dai, Lihua</au><au>Chen, Fenghua</au><au>Zheng, Yonghua</au><au>Zhang, Ding</au><au>Qian, Bao</au><au>Ji, Huaxia</au><au>Long, Feng</au><au>Cretoiu, Dragos</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-21 regulates growth and EMT in lung cancer cells via PTEN/Akt/GSK3β signaling</atitle><jtitle>Frontiers in bioscience</jtitle><addtitle>Front Biosci (Landmark Ed)</addtitle><date>2019-06-01</date><risdate>2019</risdate><volume>24</volume><issue>8</issue><spage>1426</spage><epage>1439</epage><pages>1426-1439</pages><artnum>4788</artnum><issn>1093-9946</issn><eissn>2768-6698</eissn><eissn>1093-4715</eissn><abstract>miRNA-21 (miR-21) is overexpressed in various human cancers. Here, we show that miR-21 is overexpressed in human Non-Small Cell Lung Cancer (NSCLC) and that its up or down-regulation, respectively, increases or decreases cyclin D1 and cyclin E1 expression and coordinately promotes or inhibits proliferation of cancer cells. The perturbations of miR-21 also dramatically reduces or increases epithelial to mesenschymal transition (EMT). We show that regulation of proliferation and EMT are directed by PTEN/Akt/GSK3 beta signaling axis by regulating the expression of invasion markers including E-cadherin, vimentin, snail, slug and beta-catenin. Together, these findings show that miR-21 is a potential target for the development of treatment for NSCLC forms of human lung cancer.</abstract><cop>Singapore</cop><pmid>31136988</pmid><doi>10.2741/4788</doi><tpages>14</tpages></addata></record> |
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subjects | A549 Cells Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - metabolism Carcinoma, Non-Small-Cell Lung - pathology Cell Line, Tumor Cell Proliferation - genetics Cyclins - genetics Cyclins - metabolism Epithelial-Mesenchymal Transition - genetics Gene Expression Regulation, Neoplastic Glycogen Synthase Kinase 3 beta - genetics Glycogen Synthase Kinase 3 beta - metabolism Humans Lung Neoplasms - genetics Lung Neoplasms - metabolism Lung Neoplasms - pathology MicroRNAs - genetics Proto-Oncogene Proteins c-akt - genetics Proto-Oncogene Proteins c-akt - metabolism PTEN Phosphohydrolase - genetics PTEN Phosphohydrolase - metabolism Signal Transduction - genetics |
title | miR-21 regulates growth and EMT in lung cancer cells via PTEN/Akt/GSK3β signaling |
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