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Roles of miR-200 family members in lung cancer: more than tumor suppressors
miRNAs are a class of single-stranded noncoding RNAs, which have no coding potential, but modulate many molecular mechanisms including cancer pathogenesis. miRNAs participate in cell proliferation, differentiation, apoptosis, as well as carcinogenesis or cancer progression, and their involvement in...
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Published in: | Future oncology (London, England) England), 2018-11, Vol.14 (27), p.2875-2886 |
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description | miRNAs are a class of single-stranded noncoding RNAs, which have no coding potential, but modulate many molecular mechanisms including cancer pathogenesis. miRNAs participate in cell proliferation, differentiation, apoptosis, as well as carcinogenesis or cancer progression, and their involvement in lung cancer has been recently shown. They are suggested to have bidirectional functions on important cancer-related genes so as to enhance or attenuate tumor genesis. Epithelial-mesenchymal transition (EMT) is a fundamental process which contributes to integrity of organogenesis and tissue differentiation as well as tissue repair, organ fibrosis and the progression of carcinoma, and several miRNAs were suggested to form the network regulating EMT in lung cancer, among which, miR-200 family members (miR-200a, miR-200b, miR-200c, miR-429 and miR-141) play crucial roles in the suppression of EMT.
The function of the miR-200 family in lung carcinoma initiation and progression has been clarified in recent years, but at the same time some debates about their exact functional roles appeared. In this review, we will make a summary of recent studies about the unusual functions and mechanisms of miR-200 family in lung cancer. |
doi_str_mv | 10.2217/fon-2018-0155 |
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The function of the miR-200 family in lung carcinoma initiation and progression has been clarified in recent years, but at the same time some debates about their exact functional roles appeared. In this review, we will make a summary of recent studies about the unusual functions and mechanisms of miR-200 family in lung cancer.</description><identifier>ISSN: 1479-6694</identifier><identifier>EISSN: 1744-8301</identifier><identifier>DOI: 10.2217/fon-2018-0155</identifier><identifier>PMID: 30208739</identifier><language>eng</language><publisher>England: Future Medicine Ltd</publisher><subject>Apoptosis ; Apoptosis - genetics ; Binding sites ; Biomarkers ; Carcinoma, Non-Small-Cell Lung - genetics ; Carcinoma, Non-Small-Cell Lung - pathology ; Cell Differentiation - genetics ; Cell Proliferation - genetics ; Disease Progression ; drug resistance ; EMT ; Epigenesis, Genetic ; epigenetic regulation ; Epithelial-Mesenchymal Transition - genetics ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genes, Tumor Suppressor ; Humans ; Lung cancer ; Lung Neoplasms - genetics ; Lung Neoplasms - pathology ; Medical prognosis ; Medical screening ; Metastasis ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miR-200s ; miRNAs ; NSCLC ; radiosensitivity</subject><ispartof>Future oncology (London, England), 2018-11, Vol.14 (27), p.2875-2886</ispartof><rights>2018 Future Medicine Ltd</rights><rights>Copyright Future Medicine Ltd Nov 2018</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c371t-6a1ba58cd7f1dfe98b1a1243bdba8c789a60eb8a51949a381d4ed79e51e676ef3</citedby><cites>FETCH-LOGICAL-c371t-6a1ba58cd7f1dfe98b1a1243bdba8c789a60eb8a51949a381d4ed79e51e676ef3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30208739$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Cong</creatorcontrib><creatorcontrib>Hu, Wei</creatorcontrib><creatorcontrib>Li, Lin-Lin</creatorcontrib><creatorcontrib>Wang, Yu-Xuan</creatorcontrib><creatorcontrib>Zhou, Qun</creatorcontrib><creatorcontrib>Zhang, Feng</creatorcontrib><creatorcontrib>Song-Yang, Yi-Yan</creatorcontrib><creatorcontrib>Zhu, Wei</creatorcontrib><creatorcontrib>Sun, Cheng-Chao</creatorcontrib><creatorcontrib>Li, De-Jia</creatorcontrib><title>Roles of miR-200 family members in lung cancer: more than tumor suppressors</title><title>Future oncology (London, England)</title><addtitle>Future Oncol</addtitle><description>miRNAs are a class of single-stranded noncoding RNAs, which have no coding potential, but modulate many molecular mechanisms including cancer pathogenesis. miRNAs participate in cell proliferation, differentiation, apoptosis, as well as carcinogenesis or cancer progression, and their involvement in lung cancer has been recently shown. They are suggested to have bidirectional functions on important cancer-related genes so as to enhance or attenuate tumor genesis. Epithelial-mesenchymal transition (EMT) is a fundamental process which contributes to integrity of organogenesis and tissue differentiation as well as tissue repair, organ fibrosis and the progression of carcinoma, and several miRNAs were suggested to form the network regulating EMT in lung cancer, among which, miR-200 family members (miR-200a, miR-200b, miR-200c, miR-429 and miR-141) play crucial roles in the suppression of EMT.
The function of the miR-200 family in lung carcinoma initiation and progression has been clarified in recent years, but at the same time some debates about their exact functional roles appeared. In this review, we will make a summary of recent studies about the unusual functions and mechanisms of miR-200 family in lung cancer.</description><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Binding sites</subject><subject>Biomarkers</subject><subject>Carcinoma, Non-Small-Cell Lung - genetics</subject><subject>Carcinoma, Non-Small-Cell Lung - pathology</subject><subject>Cell Differentiation - genetics</subject><subject>Cell Proliferation - genetics</subject><subject>Disease Progression</subject><subject>drug resistance</subject><subject>EMT</subject><subject>Epigenesis, Genetic</subject><subject>epigenetic regulation</subject><subject>Epithelial-Mesenchymal Transition - genetics</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes, Tumor Suppressor</subject><subject>Humans</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - pathology</subject><subject>Medical prognosis</subject><subject>Medical screening</subject><subject>Metastasis</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miR-200s</subject><subject>miRNAs</subject><subject>NSCLC</subject><subject>radiosensitivity</subject><issn>1479-6694</issn><issn>1744-8301</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNp1kE1LAzEQhoMotlaPXiXgeTXZZDeJNyl-YUEoeg7Z7ES3dD9MNof-e1O2evM0M_DMO8yD0CUlN3lOxa3ruywnVGaEFsURmlPBeSYZocep50JlZan4DJ2FsCGEC1aQUzRjJCdSMDVHr-t-CwH3DrfNOgUR7EzbbHe4hbYCH3DT4W3sPrE1nQV_h9veAx6_TIfHmHoc4jB4CKH34RydOLMNcHGoC_Tx-PC-fM5Wb08vy_tVZpmgY1YaWplC2lo4WjtQsqKG5pxVdWWkFVKZkkAlTUEVV4ZJWnOohYKCQilKcGyBrqfcwfffEcKoN330XTqp81wUSkpSsERlE2V9H4IHpwfftMbvNCV6r04ndXqvTu_VJf7qkBqrFuo_-tdVAtQEuDjG9LJtICnR05Q2Gtt08E_4D7XcfNk</recordid><startdate>20181101</startdate><enddate>20181101</enddate><creator>Liu, Cong</creator><creator>Hu, Wei</creator><creator>Li, Lin-Lin</creator><creator>Wang, Yu-Xuan</creator><creator>Zhou, Qun</creator><creator>Zhang, Feng</creator><creator>Song-Yang, Yi-Yan</creator><creator>Zhu, Wei</creator><creator>Sun, Cheng-Chao</creator><creator>Li, De-Jia</creator><general>Future Medicine Ltd</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>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>EHMNL</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20181101</creationdate><title>Roles of miR-200 family members in lung cancer: more than tumor suppressors</title><author>Liu, Cong ; Hu, Wei ; Li, Lin-Lin ; Wang, Yu-Xuan ; Zhou, Qun ; Zhang, Feng ; Song-Yang, Yi-Yan ; Zhu, Wei ; Sun, Cheng-Chao ; Li, De-Jia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c371t-6a1ba58cd7f1dfe98b1a1243bdba8c789a60eb8a51949a381d4ed79e51e676ef3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Binding sites</topic><topic>Biomarkers</topic><topic>Carcinoma, Non-Small-Cell Lung - genetics</topic><topic>Carcinoma, Non-Small-Cell Lung - pathology</topic><topic>Cell Differentiation - genetics</topic><topic>Cell Proliferation - genetics</topic><topic>Disease Progression</topic><topic>drug resistance</topic><topic>EMT</topic><topic>Epigenesis, Genetic</topic><topic>epigenetic regulation</topic><topic>Epithelial-Mesenchymal Transition - genetics</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genes, Tumor Suppressor</topic><topic>Humans</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - pathology</topic><topic>Medical prognosis</topic><topic>Medical screening</topic><topic>Metastasis</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miR-200s</topic><topic>miRNAs</topic><topic>NSCLC</topic><topic>radiosensitivity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Cong</creatorcontrib><creatorcontrib>Hu, Wei</creatorcontrib><creatorcontrib>Li, Lin-Lin</creatorcontrib><creatorcontrib>Wang, Yu-Xuan</creatorcontrib><creatorcontrib>Zhou, Qun</creatorcontrib><creatorcontrib>Zhang, Feng</creatorcontrib><creatorcontrib>Song-Yang, Yi-Yan</creatorcontrib><creatorcontrib>Zhu, Wei</creatorcontrib><creatorcontrib>Sun, Cheng-Chao</creatorcontrib><creatorcontrib>Li, De-Jia</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>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma 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)</collection><collection>ProQuest Central</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>UK & Ireland Database</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>PML(ProQuest Medical Library)</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><jtitle>Future oncology (London, England)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Cong</au><au>Hu, Wei</au><au>Li, Lin-Lin</au><au>Wang, Yu-Xuan</au><au>Zhou, Qun</au><au>Zhang, Feng</au><au>Song-Yang, Yi-Yan</au><au>Zhu, Wei</au><au>Sun, Cheng-Chao</au><au>Li, De-Jia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Roles of miR-200 family members in lung cancer: more than tumor suppressors</atitle><jtitle>Future oncology (London, England)</jtitle><addtitle>Future Oncol</addtitle><date>2018-11-01</date><risdate>2018</risdate><volume>14</volume><issue>27</issue><spage>2875</spage><epage>2886</epage><pages>2875-2886</pages><issn>1479-6694</issn><eissn>1744-8301</eissn><abstract>miRNAs are a class of single-stranded noncoding RNAs, which have no coding potential, but modulate many molecular mechanisms including cancer pathogenesis. miRNAs participate in cell proliferation, differentiation, apoptosis, as well as carcinogenesis or cancer progression, and their involvement in lung cancer has been recently shown. They are suggested to have bidirectional functions on important cancer-related genes so as to enhance or attenuate tumor genesis. Epithelial-mesenchymal transition (EMT) is a fundamental process which contributes to integrity of organogenesis and tissue differentiation as well as tissue repair, organ fibrosis and the progression of carcinoma, and several miRNAs were suggested to form the network regulating EMT in lung cancer, among which, miR-200 family members (miR-200a, miR-200b, miR-200c, miR-429 and miR-141) play crucial roles in the suppression of EMT.
The function of the miR-200 family in lung carcinoma initiation and progression has been clarified in recent years, but at the same time some debates about their exact functional roles appeared. In this review, we will make a summary of recent studies about the unusual functions and mechanisms of miR-200 family in lung cancer.</abstract><cop>England</cop><pub>Future Medicine Ltd</pub><pmid>30208739</pmid><doi>10.2217/fon-2018-0155</doi><tpages>12</tpages></addata></record> |
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subjects | Apoptosis Apoptosis - genetics Binding sites Biomarkers Carcinoma, Non-Small-Cell Lung - genetics Carcinoma, Non-Small-Cell Lung - pathology Cell Differentiation - genetics Cell Proliferation - genetics Disease Progression drug resistance EMT Epigenesis, Genetic epigenetic regulation Epithelial-Mesenchymal Transition - genetics Gene expression Gene Expression Regulation, Neoplastic Genes, Tumor Suppressor Humans Lung cancer Lung Neoplasms - genetics Lung Neoplasms - pathology Medical prognosis Medical screening Metastasis MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miR-200s miRNAs NSCLC radiosensitivity |
title | Roles of miR-200 family members in lung cancer: more than tumor suppressors |
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