File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Hsa-let-7g inhibits proliferation of hepatocellular carcinoma cells by downregulation of c-Myc and upregulation of p16 INK4A

TitleHsa-let-7g inhibits proliferation of hepatocellular carcinoma cells by downregulation of c-Myc and upregulation of p16 INK4A
Authors
Keywordsc-Myc
hepatocellular carcinoma
hsa-let-7g
p16 INK4A
Issue Date2011
PublisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
Citation
International Journal Of Cancer, 2011, v. 128 n. 2, p. 319-331 How to Cite?
AbstractzMicroRNAs (miRNAs) are endogenously expressed small noncoding RNAs that regulate approximately one-third of human genes at post-transcription level. Previous studies have shown that miRNAs were implicated in many cellular processes and participated in the progress of various tumors including hepatocellular carcinoma (HCC). Among all miRNAs, the let-7 family is well recognized to play pivotal roles in tumorigenesis by functioning as potential growth suppressor. In the present study, we aimed to investigate the role of let-7 family, particularly the hsa-let-7g, in the molecular pathogenesis of HCC. By use of MTT, qPCR, Western blotting and 2-dimensional electrophoresis (2-DE), over-expression of hsa-let-7g was found to inhibit the proliferation of HCC cell line via negative and positive regulations of c-Myc and p16 INK4A, respectively. The expression of hsa-let-7g was noted to be markedly lowered in the HepG2, Hep3B and Huh7 cells, yet higher in the Bel-7404 HCC cell line. Proliferation of HCC cell line was significantly inhibited after the transfection of hsa-let-7g mimics, while hsa-let-7g inhibitor transfection exerted an opposite effect. Concurrently, the mRNA and protein levels of c-Myc were found significantly decreased in HepG2 cells after transfection of hsa-let-7g mimics, but obviously increased in Bel-7404 cells after transfection of hsa-let-7g inhibitor. As revealed by 2-DE, a significant upregulation of p16 INK4A was revealed after the gain-of-function study using hsa-let-7g. Therefore, we suggest that hsa-let-7g may act as a tumor suppressor gene that inhibits HCC cell proliferation by downregulating the oncogene, c-Myc, and upregulating the tumor suppressor gene, p16 INK4A. Copyright © 2010 UICC.
Persistent Identifierhttp://hdl.handle.net/10722/142972
ISSN
2014 Impact Factor: 5.085
2014 SCImago Journal Rankings: 2.175
ISI Accession Number ID
Funding AgencyGrant Number
National Basic Research Program of China2010CB912800
Funding Information:

National Basic Research Program of China; Grant number: 2010CB912800

References

 

DC FieldValueLanguage
dc.contributor.authorLan, FFen_HK
dc.contributor.authorWang, Hen_HK
dc.contributor.authorChen, YCen_HK
dc.contributor.authorChan, CYen_HK
dc.contributor.authorNg, SSen_HK
dc.contributor.authorLi, Ken_HK
dc.contributor.authorXie, Den_HK
dc.contributor.authorHe, MLen_HK
dc.contributor.authorLin, MCen_HK
dc.contributor.authorKung, HFen_HK
dc.date.accessioned2011-10-28T03:00:29Z-
dc.date.available2011-10-28T03:00:29Z-
dc.date.issued2011en_HK
dc.identifier.citationInternational Journal Of Cancer, 2011, v. 128 n. 2, p. 319-331en_HK
dc.identifier.issn0020-7136en_HK
dc.identifier.urihttp://hdl.handle.net/10722/142972-
dc.description.abstractzMicroRNAs (miRNAs) are endogenously expressed small noncoding RNAs that regulate approximately one-third of human genes at post-transcription level. Previous studies have shown that miRNAs were implicated in many cellular processes and participated in the progress of various tumors including hepatocellular carcinoma (HCC). Among all miRNAs, the let-7 family is well recognized to play pivotal roles in tumorigenesis by functioning as potential growth suppressor. In the present study, we aimed to investigate the role of let-7 family, particularly the hsa-let-7g, in the molecular pathogenesis of HCC. By use of MTT, qPCR, Western blotting and 2-dimensional electrophoresis (2-DE), over-expression of hsa-let-7g was found to inhibit the proliferation of HCC cell line via negative and positive regulations of c-Myc and p16 INK4A, respectively. The expression of hsa-let-7g was noted to be markedly lowered in the HepG2, Hep3B and Huh7 cells, yet higher in the Bel-7404 HCC cell line. Proliferation of HCC cell line was significantly inhibited after the transfection of hsa-let-7g mimics, while hsa-let-7g inhibitor transfection exerted an opposite effect. Concurrently, the mRNA and protein levels of c-Myc were found significantly decreased in HepG2 cells after transfection of hsa-let-7g mimics, but obviously increased in Bel-7404 cells after transfection of hsa-let-7g inhibitor. As revealed by 2-DE, a significant upregulation of p16 INK4A was revealed after the gain-of-function study using hsa-let-7g. Therefore, we suggest that hsa-let-7g may act as a tumor suppressor gene that inhibits HCC cell proliferation by downregulating the oncogene, c-Myc, and upregulating the tumor suppressor gene, p16 INK4A. Copyright © 2010 UICC.en_HK
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/homeen_HK
dc.relation.ispartofInternational Journal of Canceren_HK
dc.rightsInternational Journal of Cancer. Copyright © John Wiley & Sons, Inc..-
dc.subjectc-Mycen_HK
dc.subjecthepatocellular carcinomaen_HK
dc.subjecthsa-let-7gen_HK
dc.subjectp16 INK4Aen_HK
dc.subject.meshCarcinoma, Hepatocellular - pathology - prevention and control-
dc.subject.meshGene Expression Regulation, Neoplastic-
dc.subject.meshLiver Neoplasms - pathology - prevention and control-
dc.subject.meshMicroRNAs - genetics - physiology-
dc.subject.meshProto-Oncogene Proteins c-myc - genetics-
dc.titleHsa-let-7g inhibits proliferation of hepatocellular carcinoma cells by downregulation of c-Myc and upregulation of p16 INK4Aen_HK
dc.typeArticleen_HK
dc.identifier.emailNg, SS: ssmng@hku.hken_HK
dc.identifier.emailLin, MC: mcllin@hkucc.hku.hken_HK
dc.identifier.authorityNg, SS=rp00767en_HK
dc.identifier.authorityLin, MC=rp00746en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/ijc.25336en_HK
dc.identifier.pmid20309945en_HK
dc.identifier.scopuseid_2-s2.0-78649561463en_HK
dc.identifier.hkuros196607en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-78649561463&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume128en_HK
dc.identifier.issue2en_HK
dc.identifier.spage319en_HK
dc.identifier.epage331en_HK
dc.identifier.isiWOS:000285263100008-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLan, FF=35484415600en_HK
dc.identifier.scopusauthoridWang, H=7501747965en_HK
dc.identifier.scopusauthoridChen, YC=7601431852en_HK
dc.identifier.scopusauthoridChan, CY=22033276600en_HK
dc.identifier.scopusauthoridNg, SS=7403358718en_HK
dc.identifier.scopusauthoridLi, K=13604752100en_HK
dc.identifier.scopusauthoridXie, D=35070710200en_HK
dc.identifier.scopusauthoridHe, ML=35080389700en_HK
dc.identifier.scopusauthoridLin, MC=7404816359en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats