Inhibition of microRNA‐214 ameliorates hepatic fibrosis and tumor incidence in platelet‐derived growth factor C transgenic mice
Differentially regulated microRNA (miRNA) are associated with hepatic fibrosis; however, their potential usefulness for blocking hepatic fibrosis has not been exploited fully. We examined the expression of miRNA in the liver of a transgenic mouse model in which platelet‐derived growth factor C (PDGF...
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creator | Okada, Hikari Honda, Masao Campbell, Jean S. Takegoshi, Kai Sakai, Yoshio Yamashita, Taro Shirasaki, Takayoshi Takabatake, Riuta Nakamura, Mikiko Tanaka, Takuji Kaneko, Shuichi |
description | Differentially regulated microRNA (miRNA) are associated with hepatic fibrosis; however, their potential usefulness for blocking hepatic fibrosis has not been exploited fully. We examined the expression of miRNA in the liver of a transgenic mouse model in which platelet‐derived growth factor C (PDGF‐C) is overexpressed (Pdgf‐c Tg), resulting in hepatic fibrosis and steatosis and the eventual development of hepatocellular carcinoma (HCC). Robust induction of miR‐214 correlated with fibrogenesis in the liver of Pdgf‐c Tg mice, atherogenic high‐fat diet‐induced NASH mice, and patients with chronic hepatitis B or C. Pdgf‐c Tg mice were injected with locked nucleic acid (LNA)‐antimiR‐214 via the tail vein using Invivofectamine 2.0 and the degree of hepatic fibrosis and tumor incidence were evaluated. Pdgf‐c Tg mice treated with LNA‐antimiR‐214 showed a marked reduction in fibrosis and tumor incidence compared with saline or LNA‐miR‐control‐injected control mice. In vitro, LNA‐antimiR‐214 significantly ameliorated TGF‐β1‐induced pro‐fibrotic gene expression in Lx‐2 cells. MiR‐214 targets a negative regulator of EGFR signaling, Mig‐6. Mimic‐miR‐214 decreased the expression of Mig‐6 and increased the levels of EGF‐mediated p‐EGFR (Y1173 and Y845) and p‐Met (Tyr1234/1235) in Huh‐7 cells. Conversely, LNA‐antimiR‐214 repressed the expression of these genes. In conclusion, miR‐214 appears to participate in the development of hepatic fibrosis by modulating the EGFR and TGF‐β signaling pathways. LNA‐antimiR‐214 is a potential therapy for the prevention of hepatic fibrosis.
MiR‐214 appears to participate in the development of hepatic fibrosis by modulating EGFR and TGF‐β signaling pathways. LNA‐anti‐miR‐214 may be a potentially therapy in the prevention of hepatic fibrosis. |
doi_str_mv | 10.1111/cas.12730 |
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MiR‐214 appears to participate in the development of hepatic fibrosis by modulating EGFR and TGF‐β signaling pathways. LNA‐anti‐miR‐214 may be a potentially therapy in the prevention of hepatic fibrosis.</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><identifier>DOI: 10.1111/cas.12730</identifier><identifier>PMID: 26122702</identifier><language>eng</language><publisher>England: John Wiley & Sons, Ltd</publisher><subject>Animals ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - pathology ; Cell Line ; Cell Line, Tumor ; Epidermal Growth Factor - genetics ; Gene Expression - genetics ; HEK293 Cells ; Hep G2 Cells ; Hepatic fibrosis ; hepatocellular carcinoma ; Humans ; Incidence ; Liver - pathology ; Liver Cirrhosis - genetics ; Liver Cirrhosis - pathology ; Liver Neoplasms - genetics ; Liver Neoplasms - pathology ; locked nucleic acid ; Lymphokines - genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic - genetics ; microRNA ; MicroRNAs - genetics ; Oligonucleotides - genetics ; Original ; Platelet-Derived Growth Factor - genetics ; platelet‐derived growth factor C ; Proto-Oncogene Proteins c-met - genetics ; Receptor, Epidermal Growth Factor - genetics ; Signal Transduction - genetics ; Transforming Growth Factor beta1 - genetics</subject><ispartof>Cancer science, 2015-09, Vol.106 (9), p.1143-1152</ispartof><rights>2015 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japanese Cancer Association.</rights><rights>2015 The Authors. Cancer Science published by Wiley Publishing Asia Pty Ltd on behalf of Japanese Cancer Association. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4582983/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4582983/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1417,11562,27924,27925,45574,45575,46052,46476,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26122702$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Okada, Hikari</creatorcontrib><creatorcontrib>Honda, Masao</creatorcontrib><creatorcontrib>Campbell, Jean S.</creatorcontrib><creatorcontrib>Takegoshi, Kai</creatorcontrib><creatorcontrib>Sakai, Yoshio</creatorcontrib><creatorcontrib>Yamashita, Taro</creatorcontrib><creatorcontrib>Shirasaki, Takayoshi</creatorcontrib><creatorcontrib>Takabatake, Riuta</creatorcontrib><creatorcontrib>Nakamura, Mikiko</creatorcontrib><creatorcontrib>Tanaka, Takuji</creatorcontrib><creatorcontrib>Kaneko, Shuichi</creatorcontrib><title>Inhibition of microRNA‐214 ameliorates hepatic fibrosis and tumor incidence in platelet‐derived growth factor C transgenic mice</title><title>Cancer science</title><addtitle>Cancer Sci</addtitle><description>Differentially regulated microRNA (miRNA) are associated with hepatic fibrosis; however, their potential usefulness for blocking hepatic fibrosis has not been exploited fully. We examined the expression of miRNA in the liver of a transgenic mouse model in which platelet‐derived growth factor C (PDGF‐C) is overexpressed (Pdgf‐c Tg), resulting in hepatic fibrosis and steatosis and the eventual development of hepatocellular carcinoma (HCC). Robust induction of miR‐214 correlated with fibrogenesis in the liver of Pdgf‐c Tg mice, atherogenic high‐fat diet‐induced NASH mice, and patients with chronic hepatitis B or C. Pdgf‐c Tg mice were injected with locked nucleic acid (LNA)‐antimiR‐214 via the tail vein using Invivofectamine 2.0 and the degree of hepatic fibrosis and tumor incidence were evaluated. Pdgf‐c Tg mice treated with LNA‐antimiR‐214 showed a marked reduction in fibrosis and tumor incidence compared with saline or LNA‐miR‐control‐injected control mice. In vitro, LNA‐antimiR‐214 significantly ameliorated TGF‐β1‐induced pro‐fibrotic gene expression in Lx‐2 cells. MiR‐214 targets a negative regulator of EGFR signaling, Mig‐6. Mimic‐miR‐214 decreased the expression of Mig‐6 and increased the levels of EGF‐mediated p‐EGFR (Y1173 and Y845) and p‐Met (Tyr1234/1235) in Huh‐7 cells. Conversely, LNA‐antimiR‐214 repressed the expression of these genes. In conclusion, miR‐214 appears to participate in the development of hepatic fibrosis by modulating the EGFR and TGF‐β signaling pathways. LNA‐antimiR‐214 is a potential therapy for the prevention of hepatic fibrosis.
MiR‐214 appears to participate in the development of hepatic fibrosis by modulating EGFR and TGF‐β signaling pathways. LNA‐anti‐miR‐214 may be a potentially therapy in the prevention of hepatic fibrosis.</description><subject>Animals</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Cell Line</subject><subject>Cell Line, Tumor</subject><subject>Epidermal Growth Factor - genetics</subject><subject>Gene Expression - genetics</subject><subject>HEK293 Cells</subject><subject>Hep G2 Cells</subject><subject>Hepatic fibrosis</subject><subject>hepatocellular carcinoma</subject><subject>Humans</subject><subject>Incidence</subject><subject>Liver - pathology</subject><subject>Liver Cirrhosis - genetics</subject><subject>Liver Cirrhosis - pathology</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - pathology</subject><subject>locked nucleic acid</subject><subject>Lymphokines - genetics</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic - genetics</subject><subject>microRNA</subject><subject>MicroRNAs - genetics</subject><subject>Oligonucleotides - genetics</subject><subject>Original</subject><subject>Platelet-Derived Growth Factor - genetics</subject><subject>platelet‐derived growth factor C</subject><subject>Proto-Oncogene Proteins c-met - genetics</subject><subject>Receptor, Epidermal Growth Factor - genetics</subject><subject>Signal Transduction - genetics</subject><subject>Transforming Growth Factor beta1 - genetics</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><recordid>eNpVkd9qFDEYxYNYbLt64QtILr2ZNv8mmbkRlqXaQrHQ6nXIJN_spswka5Jt6Z3gC_iMPolxW4vmJod8h9_5yEHoLSUntJ5Ta_IJZYqTF-iIctE3ihD5cq9V0xPODtFxzreEcCl68QodMkkZU4QdoR8XYeMHX3wMOI549jbF68_LX99_MiqwmWHyMZkCGW9ga4q3ePRDitlnbILDZTfHhH2w3kGwUBXeTtU-QakIB8nfgcPrFO_LBo_Glupe4ZJMyGsIlVYD4TU6GM2U4c3TvUBfP559WZ03l1efLlbLy-a2FS1peiMHNziwxDrRdQ4GwkbaSVC8M0B6DkMn6CCHltDWKqs4ld2onAVBurY1fIE-PHK3u2GG-h7qIpPeJj-b9KCj8fr_SfAbvY53WrQd6zteAe-fACl-20EuevbZwjSZAHGXNVVUslaqussCvfs36znk789Xw-mj4d5P8PA8p0T_qVTXSvW-Ur1a3uwF_w2F6Zh3</recordid><startdate>201509</startdate><enddate>201509</enddate><creator>Okada, Hikari</creator><creator>Honda, Masao</creator><creator>Campbell, Jean S.</creator><creator>Takegoshi, Kai</creator><creator>Sakai, Yoshio</creator><creator>Yamashita, Taro</creator><creator>Shirasaki, Takayoshi</creator><creator>Takabatake, Riuta</creator><creator>Nakamura, Mikiko</creator><creator>Tanaka, Takuji</creator><creator>Kaneko, Shuichi</creator><general>John Wiley & Sons, Ltd</general><scope>24P</scope><scope>WIN</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201509</creationdate><title>Inhibition of microRNA‐214 ameliorates hepatic fibrosis and tumor incidence in platelet‐derived growth factor C transgenic mice</title><author>Okada, Hikari ; Honda, Masao ; Campbell, Jean S. ; Takegoshi, Kai ; Sakai, Yoshio ; Yamashita, Taro ; Shirasaki, Takayoshi ; Takabatake, Riuta ; Nakamura, Mikiko ; Tanaka, Takuji ; Kaneko, Shuichi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-j5450-9a6bdbdec0cd488deb02f186e738ae093eb841b6b5015c7c73168f7dce40855a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Cell Line</topic><topic>Cell Line, Tumor</topic><topic>Epidermal Growth Factor - genetics</topic><topic>Gene Expression - genetics</topic><topic>HEK293 Cells</topic><topic>Hep G2 Cells</topic><topic>Hepatic fibrosis</topic><topic>hepatocellular carcinoma</topic><topic>Humans</topic><topic>Incidence</topic><topic>Liver - pathology</topic><topic>Liver Cirrhosis - genetics</topic><topic>Liver Cirrhosis - pathology</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - pathology</topic><topic>locked nucleic acid</topic><topic>Lymphokines - genetics</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic - genetics</topic><topic>microRNA</topic><topic>MicroRNAs - genetics</topic><topic>Oligonucleotides - genetics</topic><topic>Original</topic><topic>Platelet-Derived Growth Factor - genetics</topic><topic>platelet‐derived growth factor C</topic><topic>Proto-Oncogene Proteins c-met - genetics</topic><topic>Receptor, Epidermal Growth Factor - genetics</topic><topic>Signal Transduction - genetics</topic><topic>Transforming Growth Factor beta1 - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Okada, Hikari</creatorcontrib><creatorcontrib>Honda, Masao</creatorcontrib><creatorcontrib>Campbell, Jean S.</creatorcontrib><creatorcontrib>Takegoshi, Kai</creatorcontrib><creatorcontrib>Sakai, Yoshio</creatorcontrib><creatorcontrib>Yamashita, Taro</creatorcontrib><creatorcontrib>Shirasaki, Takayoshi</creatorcontrib><creatorcontrib>Takabatake, Riuta</creatorcontrib><creatorcontrib>Nakamura, Mikiko</creatorcontrib><creatorcontrib>Tanaka, Takuji</creatorcontrib><creatorcontrib>Kaneko, Shuichi</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library (Open Access Collection)</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Okada, Hikari</au><au>Honda, Masao</au><au>Campbell, Jean S.</au><au>Takegoshi, Kai</au><au>Sakai, Yoshio</au><au>Yamashita, Taro</au><au>Shirasaki, Takayoshi</au><au>Takabatake, Riuta</au><au>Nakamura, Mikiko</au><au>Tanaka, Takuji</au><au>Kaneko, Shuichi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of microRNA‐214 ameliorates hepatic fibrosis and tumor incidence in platelet‐derived growth factor C transgenic mice</atitle><jtitle>Cancer science</jtitle><addtitle>Cancer Sci</addtitle><date>2015-09</date><risdate>2015</risdate><volume>106</volume><issue>9</issue><spage>1143</spage><epage>1152</epage><pages>1143-1152</pages><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>Differentially regulated microRNA (miRNA) are associated with hepatic fibrosis; however, their potential usefulness for blocking hepatic fibrosis has not been exploited fully. We examined the expression of miRNA in the liver of a transgenic mouse model in which platelet‐derived growth factor C (PDGF‐C) is overexpressed (Pdgf‐c Tg), resulting in hepatic fibrosis and steatosis and the eventual development of hepatocellular carcinoma (HCC). Robust induction of miR‐214 correlated with fibrogenesis in the liver of Pdgf‐c Tg mice, atherogenic high‐fat diet‐induced NASH mice, and patients with chronic hepatitis B or C. Pdgf‐c Tg mice were injected with locked nucleic acid (LNA)‐antimiR‐214 via the tail vein using Invivofectamine 2.0 and the degree of hepatic fibrosis and tumor incidence were evaluated. Pdgf‐c Tg mice treated with LNA‐antimiR‐214 showed a marked reduction in fibrosis and tumor incidence compared with saline or LNA‐miR‐control‐injected control mice. In vitro, LNA‐antimiR‐214 significantly ameliorated TGF‐β1‐induced pro‐fibrotic gene expression in Lx‐2 cells. MiR‐214 targets a negative regulator of EGFR signaling, Mig‐6. Mimic‐miR‐214 decreased the expression of Mig‐6 and increased the levels of EGF‐mediated p‐EGFR (Y1173 and Y845) and p‐Met (Tyr1234/1235) in Huh‐7 cells. Conversely, LNA‐antimiR‐214 repressed the expression of these genes. In conclusion, miR‐214 appears to participate in the development of hepatic fibrosis by modulating the EGFR and TGF‐β signaling pathways. LNA‐antimiR‐214 is a potential therapy for the prevention of hepatic fibrosis.
MiR‐214 appears to participate in the development of hepatic fibrosis by modulating EGFR and TGF‐β signaling pathways. LNA‐anti‐miR‐214 may be a potentially therapy in the prevention of hepatic fibrosis.</abstract><cop>England</cop><pub>John Wiley & Sons, Ltd</pub><pmid>26122702</pmid><doi>10.1111/cas.12730</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - pathology Cell Line Cell Line, Tumor Epidermal Growth Factor - genetics Gene Expression - genetics HEK293 Cells Hep G2 Cells Hepatic fibrosis hepatocellular carcinoma Humans Incidence Liver - pathology Liver Cirrhosis - genetics Liver Cirrhosis - pathology Liver Neoplasms - genetics Liver Neoplasms - pathology locked nucleic acid Lymphokines - genetics Male Mice Mice, Inbred C57BL Mice, Transgenic - genetics microRNA MicroRNAs - genetics Oligonucleotides - genetics Original Platelet-Derived Growth Factor - genetics platelet‐derived growth factor C Proto-Oncogene Proteins c-met - genetics Receptor, Epidermal Growth Factor - genetics Signal Transduction - genetics Transforming Growth Factor beta1 - genetics |
title | Inhibition of microRNA‐214 ameliorates hepatic fibrosis and tumor incidence in platelet‐derived growth factor C transgenic mice |
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