MicroRNA-34c targets TGFB-induced factor homeobox 2, represses cell proliferation and induces apoptosis in hepatitis B virus-related hepatocellular carcinoma
MicroRNAs (miRs) are short, non-coding RNAs with post-transcriptional regulatory functions. Previous studies have demonstrated that miR-34c is involved in diverse biological processes, including carcinogenesis. The aim of the present study was to investigate the role of miR-34c and its target genes...
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| Veröffentlicht in: | Oncology letters 2015-11, Vol.10 (5), p.3095-3102 |
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| creator | WANG, YAN WANG, CHUN-MEI JIANG, ZHEN-ZHONG YU, XIAO-JIAN FAN, CHUN-GUANG XU, FEI-FEI ZHANG, QING LI, LI LI, RUI-FENG SUN, WEN-SHENG ZHANG, ZHEN-HAI LIU, YU-GANG |
| description | MicroRNAs (miRs) are short, non-coding RNAs with post-transcriptional regulatory functions. Previous studies have demonstrated that miR-34c is involved in diverse biological processes, including carcinogenesis. The aim of the present study was to investigate the role of miR-34c and its target genes in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). Expression levels of miR-34c and its predicted target genes were measured. The target genes were validated by a luciferase assay. The effects of miR-34c restoration were evaluated by the detection of HBV antigens, cell proliferation and apoptosis in vitro, in addition to the tumor growth in vivo. The data demonstrated that miR-34c was downregulated in HBV-associated HCC clinical tissues and HCC cell lines compared with their corresponding controls. transforming growth factor-β-induced factor homeobox 2 (TGIF2), a transcription factor repressing transforming growth factor-β (TGFβ) signaling, was observed to be upregulated and was identified as a target gene of miR-34c. The restoration of miR-34c in HepG2.2.15 cells suppressed TGIF2 expression, HBV replication and viral antigen synthesis; inhibited cell proliferation; and induced apoptosis. miR-34c also inhibited tumor growth in a mouse model. The present study indicates that miR-34c may act as a tumor suppressor by targeting TGIF2 during HBV-associated hepatocellular carcinogenesis. miR-34c and TGIF2 may represent key regulatory factors, diagnostic markers and therapeutic targets for the prevention and treatment of HBV-associated HCC. |
| doi_str_mv | 10.3892/ol.2015.3649 |
| format | Article |
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Previous studies have demonstrated that miR-34c is involved in diverse biological processes, including carcinogenesis. The aim of the present study was to investigate the role of miR-34c and its target genes in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). Expression levels of miR-34c and its predicted target genes were measured. The target genes were validated by a luciferase assay. The effects of miR-34c restoration were evaluated by the detection of HBV antigens, cell proliferation and apoptosis in vitro, in addition to the tumor growth in vivo. The data demonstrated that miR-34c was downregulated in HBV-associated HCC clinical tissues and HCC cell lines compared with their corresponding controls. transforming growth factor-β-induced factor homeobox 2 (TGIF2), a transcription factor repressing transforming growth factor-β (TGFβ) signaling, was observed to be upregulated and was identified as a target gene of miR-34c. The restoration of miR-34c in HepG2.2.15 cells suppressed TGIF2 expression, HBV replication and viral antigen synthesis; inhibited cell proliferation; and induced apoptosis. miR-34c also inhibited tumor growth in a mouse model. The present study indicates that miR-34c may act as a tumor suppressor by targeting TGIF2 during HBV-associated hepatocellular carcinogenesis. miR-34c and TGIF2 may represent key regulatory factors, diagnostic markers and therapeutic targets for the prevention and treatment of HBV-associated HCC.</description><identifier>ISSN: 1792-1074</identifier><identifier>EISSN: 1792-1082</identifier><identifier>DOI: 10.3892/ol.2015.3649</identifier><identifier>PMID: 26722295</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Antigens ; Apoptosis ; Bioinformatics ; Cell cycle ; Cell growth ; Deoxyribonucleic acid ; Development and progression ; DNA ; Enzymes ; Gene expression ; Genetic aspects ; Growth factors ; Health aspects ; Hepatitis ; Hepatitis B ; hepatitis B virus ; hepatocellular carcinoma ; Hepatoma ; Kinases ; Liver cancer ; MicroRNA ; microRNA-34c ; MicroRNAs ; Oncology ; Plasmids ; Properties ; Proteins ; Rodents ; Studies ; TGFB-induced factor homeobox 2 ; Transforming growth factors ; Tumorigenesis</subject><ispartof>Oncology letters, 2015-11, Vol.10 (5), p.3095-3102</ispartof><rights>Copyright © 2015, Spandidos Publications</rights><rights>COPYRIGHT 2015 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2015</rights><rights>Copyright © 2015, Spandidos Publications 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c605t-90788c4b0894486782f07c10216de95a453df67427dc70c24e40d2e5093bbd353</citedby><cites>FETCH-LOGICAL-c605t-90788c4b0894486782f07c10216de95a453df67427dc70c24e40d2e5093bbd353</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4665706/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4665706/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,5555,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26722295$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>WANG, YAN</creatorcontrib><creatorcontrib>WANG, CHUN-MEI</creatorcontrib><creatorcontrib>JIANG, ZHEN-ZHONG</creatorcontrib><creatorcontrib>YU, XIAO-JIAN</creatorcontrib><creatorcontrib>FAN, CHUN-GUANG</creatorcontrib><creatorcontrib>XU, FEI-FEI</creatorcontrib><creatorcontrib>ZHANG, QING</creatorcontrib><creatorcontrib>LI, LI</creatorcontrib><creatorcontrib>LI, RUI-FENG</creatorcontrib><creatorcontrib>SUN, WEN-SHENG</creatorcontrib><creatorcontrib>ZHANG, ZHEN-HAI</creatorcontrib><creatorcontrib>LIU, YU-GANG</creatorcontrib><title>MicroRNA-34c targets TGFB-induced factor homeobox 2, represses cell proliferation and induces apoptosis in hepatitis B virus-related hepatocellular carcinoma</title><title>Oncology letters</title><addtitle>Oncol Lett</addtitle><description>MicroRNAs (miRs) are short, non-coding RNAs with post-transcriptional regulatory functions. Previous studies have demonstrated that miR-34c is involved in diverse biological processes, including carcinogenesis. The aim of the present study was to investigate the role of miR-34c and its target genes in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). Expression levels of miR-34c and its predicted target genes were measured. The target genes were validated by a luciferase assay. The effects of miR-34c restoration were evaluated by the detection of HBV antigens, cell proliferation and apoptosis in vitro, in addition to the tumor growth in vivo. The data demonstrated that miR-34c was downregulated in HBV-associated HCC clinical tissues and HCC cell lines compared with their corresponding controls. transforming growth factor-β-induced factor homeobox 2 (TGIF2), a transcription factor repressing transforming growth factor-β (TGFβ) signaling, was observed to be upregulated and was identified as a target gene of miR-34c. The restoration of miR-34c in HepG2.2.15 cells suppressed TGIF2 expression, HBV replication and viral antigen synthesis; inhibited cell proliferation; and induced apoptosis. miR-34c also inhibited tumor growth in a mouse model. The present study indicates that miR-34c may act as a tumor suppressor by targeting TGIF2 during HBV-associated hepatocellular carcinogenesis. miR-34c and TGIF2 may represent key regulatory factors, diagnostic markers and therapeutic targets for the prevention and treatment of HBV-associated HCC.</description><subject>Antigens</subject><subject>Apoptosis</subject><subject>Bioinformatics</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Deoxyribonucleic acid</subject><subject>Development and progression</subject><subject>DNA</subject><subject>Enzymes</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Growth factors</subject><subject>Health aspects</subject><subject>Hepatitis</subject><subject>Hepatitis B</subject><subject>hepatitis B virus</subject><subject>hepatocellular carcinoma</subject><subject>Hepatoma</subject><subject>Kinases</subject><subject>Liver cancer</subject><subject>MicroRNA</subject><subject>microRNA-34c</subject><subject>MicroRNAs</subject><subject>Oncology</subject><subject>Plasmids</subject><subject>Properties</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Studies</subject><subject>TGFB-induced factor homeobox 2</subject><subject>Transforming growth factors</subject><subject>Tumorigenesis</subject><issn>1792-1074</issn><issn>1792-1082</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkk1v1DAQhiMEolXpjTOyBEIcmsWxHce-IG0rWpAWKqFytrz2pOvKiYOdVPBj-K843bLaRdgHf8wzrzXjtyheVnhBhSTvg18QXNULypl8UhxXjSRlhQV5uts37Kg4TekO51HzSgj-vDgivCGEyPq4-P3FmRi-fV2WlBk06ngLY0I3V5fnpevtZMCiVpsxRLQJHYR1-InIGYowREgJEjLgPRpi8K6FqEcXeqR7i7a5CekhDGNILuUbtIEhE2M-nKN7F6dURvB6zE88RMKsNXkdkdHRuD50-kXxrNU-wenjelJ8v_x4c_GpXF1ffb5YrkrDcT2WEjdCGLbGQjImeCNIixtTYVJxC7LWrKa25Q0jjTUNNoQBw5ZAjSVdry2t6UnxYas7TOsOrIF-jNqrIbpOx18qaKcOI73bqNtwrxjndYN5Fnj3KBDDjwnSqDqX5np0D2FKqhKEcyaYlBl9_Q96F6bY5_JUJSnJeg3do261B-X6NuR3zSyqlizHCaaYZmrxHypPC50zoYfW5fuDhLd7CRvQftyk4Kf549IheLYFsztSitDumlFhNVtPBa9m66nZehl_td_AHfzXaBl4swXSkP3hbEg75npV4jwfdP4Akh7fRA</recordid><startdate>20151101</startdate><enddate>20151101</enddate><creator>WANG, YAN</creator><creator>WANG, CHUN-MEI</creator><creator>JIANG, ZHEN-ZHONG</creator><creator>YU, XIAO-JIAN</creator><creator>FAN, CHUN-GUANG</creator><creator>XU, FEI-FEI</creator><creator>ZHANG, QING</creator><creator>LI, LI</creator><creator>LI, RUI-FENG</creator><creator>SUN, WEN-SHENG</creator><creator>ZHANG, ZHEN-HAI</creator><creator>LIU, YU-GANG</creator><general>D.A. 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>WANG, YAN</au><au>WANG, CHUN-MEI</au><au>JIANG, ZHEN-ZHONG</au><au>YU, XIAO-JIAN</au><au>FAN, CHUN-GUANG</au><au>XU, FEI-FEI</au><au>ZHANG, QING</au><au>LI, LI</au><au>LI, RUI-FENG</au><au>SUN, WEN-SHENG</au><au>ZHANG, ZHEN-HAI</au><au>LIU, YU-GANG</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA-34c targets TGFB-induced factor homeobox 2, represses cell proliferation and induces apoptosis in hepatitis B virus-related hepatocellular carcinoma</atitle><jtitle>Oncology letters</jtitle><addtitle>Oncol Lett</addtitle><date>2015-11-01</date><risdate>2015</risdate><volume>10</volume><issue>5</issue><spage>3095</spage><epage>3102</epage><pages>3095-3102</pages><issn>1792-1074</issn><eissn>1792-1082</eissn><abstract>MicroRNAs (miRs) are short, non-coding RNAs with post-transcriptional regulatory functions. Previous studies have demonstrated that miR-34c is involved in diverse biological processes, including carcinogenesis. The aim of the present study was to investigate the role of miR-34c and its target genes in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). Expression levels of miR-34c and its predicted target genes were measured. The target genes were validated by a luciferase assay. The effects of miR-34c restoration were evaluated by the detection of HBV antigens, cell proliferation and apoptosis in vitro, in addition to the tumor growth in vivo. The data demonstrated that miR-34c was downregulated in HBV-associated HCC clinical tissues and HCC cell lines compared with their corresponding controls. transforming growth factor-β-induced factor homeobox 2 (TGIF2), a transcription factor repressing transforming growth factor-β (TGFβ) signaling, was observed to be upregulated and was identified as a target gene of miR-34c. The restoration of miR-34c in HepG2.2.15 cells suppressed TGIF2 expression, HBV replication and viral antigen synthesis; inhibited cell proliferation; and induced apoptosis. miR-34c also inhibited tumor growth in a mouse model. The present study indicates that miR-34c may act as a tumor suppressor by targeting TGIF2 during HBV-associated hepatocellular carcinogenesis. miR-34c and TGIF2 may represent key regulatory factors, diagnostic markers and therapeutic targets for the prevention and treatment of HBV-associated HCC.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>26722295</pmid><doi>10.3892/ol.2015.3649</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Antigens Apoptosis Bioinformatics Cell cycle Cell growth Deoxyribonucleic acid Development and progression DNA Enzymes Gene expression Genetic aspects Growth factors Health aspects Hepatitis Hepatitis B hepatitis B virus hepatocellular carcinoma Hepatoma Kinases Liver cancer MicroRNA microRNA-34c MicroRNAs Oncology Plasmids Properties Proteins Rodents Studies TGFB-induced factor homeobox 2 Transforming growth factors Tumorigenesis |
| title | MicroRNA-34c targets TGFB-induced factor homeobox 2, represses cell proliferation and induces apoptosis in hepatitis B virus-related hepatocellular carcinoma |
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