Down‐regulation of miR‐214 contributes to intrahepatic cholangiocarcinoma metastasis by targeting Twist
miRNAs play an important role in many human diseases, including cancer metastasis. However, the mechanisms by which miRNAs regulate intrahepatic cholangiocarcinoma metastasis remain poorly understood. In the present study, we assayed the expression level of miR‐214 in intrahepatic cholangiocarcinoma...
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description | miRNAs play an important role in many human diseases, including cancer metastasis. However, the mechanisms by which miRNAs regulate intrahepatic cholangiocarcinoma metastasis remain poorly understood. In the present study, we assayed the expression level of miR‐214 in intrahepatic cholangiocarcinoma tissues by real‐time PCR, and defined the target gene and biological function by luciferase reporter assay and Western blot analysis. We found that the miR‐214 levels were remarkably decreased in metastatic intrahepatic cholangiocarcinoma tissues compared to non‐metastatic tissues. Inhibition of miR‐214 levels by its inhibitor promoted metastasis of human intrahepatic cholangiocarcinoma cell. We further demonstrated that down‐regulation of miR‐214 increased the transcript levels of the epithelial–mesenchymal transition‐associated gene Twist, and then decreased E‐cadherin levels. We confirmed that down‐regulation of miR‐214 promoted the epithelial–mesenchymal transition by directly targeting the Twist gene. These results suggest an important role for miR‐214 in regulating metastasis of intrahepatic cholangiocarcinoma, and potential application of miR‐214 in intrahepatic cholangiocarcinoma therapy.
miR‐214 levels were remarkably decreased in metastatic intrahepatic cholangiocarcinoma tissues compared to non‐metastatic tissues. Inhibition of miR‐214 levels by its inhibitor promoted metastasis of human intrahepatic cholangiocarcinoma cells. Downregulated miR‐214 increased the levels of the EMT‐associated gene Twist, and decreased E‐cadherin levels. We confirmed that downregulated miR‐214 promoted EMT by directly targeting the Twist gene. |
doi_str_mv | 10.1111/j.1742-4658.2012.08618.x |
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miR‐214 levels were remarkably decreased in metastatic intrahepatic cholangiocarcinoma tissues compared to non‐metastatic tissues. Inhibition of miR‐214 levels by its inhibitor promoted metastasis of human intrahepatic cholangiocarcinoma cells. Downregulated miR‐214 increased the levels of the EMT‐associated gene Twist, and decreased E‐cadherin levels. We confirmed that downregulated miR‐214 promoted EMT by directly targeting the Twist gene.</description><identifier>ISSN: 1742-464X</identifier><identifier>EISSN: 1742-4658</identifier><identifier>DOI: 10.1111/j.1742-4658.2012.08618.x</identifier><identifier>PMID: 22540680</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Bile Duct Neoplasms ; Bile Ducts, Intrahepatic ; Biochemistry ; Blotting, Western ; Cancer ; Cell Line, Tumor ; Cell Movement ; Cholangiocarcinoma - genetics ; Cholangiocarcinoma - metabolism ; Cholangiocarcinoma - secondary ; Down-Regulation ; Epithelial-Mesenchymal Transition ; E‐cadherin ; Gene Expression Regulation, Neoplastic - genetics ; Humans ; intrahepatic cholangiocarcinoma ; Liver Neoplasms - genetics ; Liver Neoplasms - metabolism ; Liver Neoplasms - secondary ; Luciferases - metabolism ; Metastasis ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miR214 ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Ribonucleic acid ; RNA ; RNA, Messenger - genetics ; Twist ; Twist-Related Protein 1 - genetics ; Twist-Related Protein 1 - metabolism</subject><ispartof>The FEBS journal, 2012-07, Vol.279 (13), p.2393-2398</ispartof><rights>2012 The Authors Journal compilation © 2012 FEBS</rights><rights>2012 The Authors Journal compilation © 2012 FEBS.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5148-9e501b843fc63468dc9bd1686b9a0b2a9648f7a4f5f17c8f868fab1a471306023</citedby><cites>FETCH-LOGICAL-c5148-9e501b843fc63468dc9bd1686b9a0b2a9648f7a4f5f17c8f868fab1a471306023</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1742-4658.2012.08618.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1742-4658.2012.08618.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,1434,27928,27929,45578,45579,46413,46837</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22540680$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Bin</creatorcontrib><creatorcontrib>Han, Qingqi</creatorcontrib><creatorcontrib>Zhu, Yan</creatorcontrib><creatorcontrib>Yu, Yong</creatorcontrib><creatorcontrib>Wang, Jinghan</creatorcontrib><creatorcontrib>Jiang, Xiaoqing</creatorcontrib><title>Down‐regulation of miR‐214 contributes to intrahepatic cholangiocarcinoma metastasis by targeting Twist</title><title>The FEBS journal</title><addtitle>FEBS J</addtitle><description>miRNAs play an important role in many human diseases, including cancer metastasis. However, the mechanisms by which miRNAs regulate intrahepatic cholangiocarcinoma metastasis remain poorly understood. In the present study, we assayed the expression level of miR‐214 in intrahepatic cholangiocarcinoma tissues by real‐time PCR, and defined the target gene and biological function by luciferase reporter assay and Western blot analysis. We found that the miR‐214 levels were remarkably decreased in metastatic intrahepatic cholangiocarcinoma tissues compared to non‐metastatic tissues. Inhibition of miR‐214 levels by its inhibitor promoted metastasis of human intrahepatic cholangiocarcinoma cell. We further demonstrated that down‐regulation of miR‐214 increased the transcript levels of the epithelial–mesenchymal transition‐associated gene Twist, and then decreased E‐cadherin levels. We confirmed that down‐regulation of miR‐214 promoted the epithelial–mesenchymal transition by directly targeting the Twist gene. These results suggest an important role for miR‐214 in regulating metastasis of intrahepatic cholangiocarcinoma, and potential application of miR‐214 in intrahepatic cholangiocarcinoma therapy.
miR‐214 levels were remarkably decreased in metastatic intrahepatic cholangiocarcinoma tissues compared to non‐metastatic tissues. Inhibition of miR‐214 levels by its inhibitor promoted metastasis of human intrahepatic cholangiocarcinoma cells. Downregulated miR‐214 increased the levels of the EMT‐associated gene Twist, and decreased E‐cadherin levels. We confirmed that downregulated miR‐214 promoted EMT by directly targeting the Twist gene.</description><subject>Bile Duct Neoplasms</subject><subject>Bile Ducts, Intrahepatic</subject><subject>Biochemistry</subject><subject>Blotting, Western</subject><subject>Cancer</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cholangiocarcinoma - genetics</subject><subject>Cholangiocarcinoma - metabolism</subject><subject>Cholangiocarcinoma - secondary</subject><subject>Down-Regulation</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>E‐cadherin</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Humans</subject><subject>intrahepatic cholangiocarcinoma</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - metabolism</subject><subject>Liver Neoplasms - secondary</subject><subject>Luciferases - metabolism</subject><subject>Metastasis</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miR214</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Messenger - genetics</subject><subject>Twist</subject><subject>Twist-Related Protein 1 - genetics</subject><subject>Twist-Related Protein 1 - metabolism</subject><issn>1742-464X</issn><issn>1742-4658</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkcFuGyEQhlGUqnHTvkKElEsu3gALmL1ESl2nqRQpUppKvSEWg4OzuzjAyvGtj5Bn7JOEjR0feipCYoBvZn7NDwDEqMB5nS8LPKFkTDkTBUGYFEhwLIrnAzDafxzuY_r7CHyKcYlQyWhVfQRHhDCKuEAj8PjNr7u_f16CWfSNSs530FvYurv8RjCF2ncpuLpPJsLkocs39WBWmdRQP_hGdQvntQradb5VsDVJxbxdhPUGJhUWJrluAe_XLqbP4INVTTRfducx-HU1u59ej29uv_-YXt6MNcNUjCvDEK4FLa3mJeVirqt6jrngdaVQTVTFqbATRS2zeKKFFVxYVWNFJ7hEHJHyGJxt666Cf-pNTLJ1UZsmizW-jxIjgjFh4g09_Qdd-j50Wd1AIcaqLCBTYkvp4GMMxspVcK0KmwzJwRC5lMOs5TB3ORgi3wyRzzn1ZNegr1sz3ye-O5CBiy2wdo3Z_HdheTX7-nMIy1eoN5wL</recordid><startdate>201207</startdate><enddate>201207</enddate><creator>Li, Bin</creator><creator>Han, Qingqi</creator><creator>Zhu, Yan</creator><creator>Yu, Yong</creator><creator>Wang, Jinghan</creator><creator>Jiang, Xiaoqing</creator><general>Blackwell Publishing 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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>201207</creationdate><title>Down‐regulation of miR‐214 contributes to intrahepatic cholangiocarcinoma metastasis by targeting Twist</title><author>Li, Bin ; Han, Qingqi ; Zhu, Yan ; Yu, Yong ; Wang, Jinghan ; Jiang, Xiaoqing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5148-9e501b843fc63468dc9bd1686b9a0b2a9648f7a4f5f17c8f868fab1a471306023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Bile Duct Neoplasms</topic><topic>Bile Ducts, Intrahepatic</topic><topic>Biochemistry</topic><topic>Blotting, Western</topic><topic>Cancer</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cholangiocarcinoma - genetics</topic><topic>Cholangiocarcinoma - metabolism</topic><topic>Cholangiocarcinoma - secondary</topic><topic>Down-Regulation</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>E‐cadherin</topic><topic>Gene Expression Regulation, Neoplastic - genetics</topic><topic>Humans</topic><topic>intrahepatic cholangiocarcinoma</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - metabolism</topic><topic>Liver Neoplasms - secondary</topic><topic>Luciferases - metabolism</topic><topic>Metastasis</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miR214</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Messenger - genetics</topic><topic>Twist</topic><topic>Twist-Related Protein 1 - genetics</topic><topic>Twist-Related Protein 1 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Bin</creatorcontrib><creatorcontrib>Han, Qingqi</creatorcontrib><creatorcontrib>Zhu, Yan</creatorcontrib><creatorcontrib>Yu, Yong</creatorcontrib><creatorcontrib>Wang, Jinghan</creatorcontrib><creatorcontrib>Jiang, Xiaoqing</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The FEBS journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Bin</au><au>Han, Qingqi</au><au>Zhu, Yan</au><au>Yu, Yong</au><au>Wang, Jinghan</au><au>Jiang, Xiaoqing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Down‐regulation of miR‐214 contributes to intrahepatic cholangiocarcinoma metastasis by targeting Twist</atitle><jtitle>The FEBS journal</jtitle><addtitle>FEBS J</addtitle><date>2012-07</date><risdate>2012</risdate><volume>279</volume><issue>13</issue><spage>2393</spage><epage>2398</epage><pages>2393-2398</pages><issn>1742-464X</issn><eissn>1742-4658</eissn><abstract>miRNAs play an important role in many human diseases, including cancer metastasis. However, the mechanisms by which miRNAs regulate intrahepatic cholangiocarcinoma metastasis remain poorly understood. In the present study, we assayed the expression level of miR‐214 in intrahepatic cholangiocarcinoma tissues by real‐time PCR, and defined the target gene and biological function by luciferase reporter assay and Western blot analysis. We found that the miR‐214 levels were remarkably decreased in metastatic intrahepatic cholangiocarcinoma tissues compared to non‐metastatic tissues. Inhibition of miR‐214 levels by its inhibitor promoted metastasis of human intrahepatic cholangiocarcinoma cell. We further demonstrated that down‐regulation of miR‐214 increased the transcript levels of the epithelial–mesenchymal transition‐associated gene Twist, and then decreased E‐cadherin levels. We confirmed that down‐regulation of miR‐214 promoted the epithelial–mesenchymal transition by directly targeting the Twist gene. These results suggest an important role for miR‐214 in regulating metastasis of intrahepatic cholangiocarcinoma, and potential application of miR‐214 in intrahepatic cholangiocarcinoma therapy.
miR‐214 levels were remarkably decreased in metastatic intrahepatic cholangiocarcinoma tissues compared to non‐metastatic tissues. Inhibition of miR‐214 levels by its inhibitor promoted metastasis of human intrahepatic cholangiocarcinoma cells. Downregulated miR‐214 increased the levels of the EMT‐associated gene Twist, and decreased E‐cadherin levels. We confirmed that downregulated miR‐214 promoted EMT by directly targeting the Twist gene.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>22540680</pmid><doi>10.1111/j.1742-4658.2012.08618.x</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Bile Duct Neoplasms Bile Ducts, Intrahepatic Biochemistry Blotting, Western Cancer Cell Line, Tumor Cell Movement Cholangiocarcinoma - genetics Cholangiocarcinoma - metabolism Cholangiocarcinoma - secondary Down-Regulation Epithelial-Mesenchymal Transition E‐cadherin Gene Expression Regulation, Neoplastic - genetics Humans intrahepatic cholangiocarcinoma Liver Neoplasms - genetics Liver Neoplasms - metabolism Liver Neoplasms - secondary Luciferases - metabolism Metastasis MicroRNAs - genetics MicroRNAs - metabolism miR214 Nuclear Proteins - genetics Nuclear Proteins - metabolism Real-Time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction Ribonucleic acid RNA RNA, Messenger - genetics Twist Twist-Related Protein 1 - genetics Twist-Related Protein 1 - metabolism |
title | Down‐regulation of miR‐214 contributes to intrahepatic cholangiocarcinoma metastasis by targeting Twist |
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