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Article: MicroRNA let-7 suppresses nasopharyngeal carcinoma cells proliferation through downregulating c-Myc expression

TitleMicroRNA let-7 suppresses nasopharyngeal carcinoma cells proliferation through downregulating c-Myc expression
Authors
KeywordsEpigenetic regulation
Let-7
MicroRNAs
Nasopharyngeal carcinoma
Proliferation
Issue Date2011
PublisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00432/index.htm
Citation
Journal Of Cancer Research And Clinical Oncology, 2011, v. 137 n. 3, p. 415-422 How to Cite?
AbstractAims: This study aimed at evaluating the potential anti-proliferative effects of the microRNA let-7 family in nasopharyngeal carcinoma (NPC) cells. In addition, the association between let-7 suppression and DNA hypermethylation is examined. Materials and methods: Levels of mature let-7 family members (-a,-b,-d,-e,-g, and-i) in normal nasopharyngeal cells (NP69 and NP460) and nasopharyngeal carcinoma cells (HK1 and HONE1) were measured by real-time quantitative PCR. Cell-proliferation assay and c-Myc immunohistochemical staining were performed on NPC cells transfected with let-7 precursor molecules. In addition, expression changes in let-7 family members in response to demethylating agents (5-azacytidine and zebularine) were also examined. Results: In comparison with the normal nasopharyngeal cells, let-7 (-a,-b,-d,-e,-g, and-i) levels were reduced in nasopharyngeal carcinoma cells. Ectopic expression of the let-7 family in nasopharyngeal carcinoma cells resulted in inhibition of cell proliferation through downregulation of c-Myc expression. Demethylation treatment of nasopharyngeal carcinoma cells caused activation of let-7 expression in poorly differentiated nasopharyngeal carcinoma cells only. Conclusion: Our results suggested that miRNA let-7 might play a role in the proliferation of NPC. DNA methylation is a potential regulatory pathway, which is affected when let-7 is suppressed in NPC cells. However, the extent of DNA hypermethylation/hypomethylation in regulating let-7 expression requires further elucidation. © The Author(s) 2010. This article is published with open access at Springerlink.com.
Persistent Identifierhttp://hdl.handle.net/10722/145040
ISSN
2015 Impact Factor: 3.141
2015 SCImago Journal Rankings: 1.190
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
University of Hong Kong, Hong Kong, China
Funding Information:

The study was supported by Seed Funding for Basic research, The University of Hong Kong, Hong Kong, China.

References

 

DC FieldValueLanguage
dc.contributor.authorWong, TSen_HK
dc.contributor.authorMan, OYen_HK
dc.contributor.authorTsang, CMen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorTsang, RKYen_HK
dc.contributor.authorChan, JYWen_HK
dc.contributor.authorHo, WKen_HK
dc.contributor.authorWei, WIen_HK
dc.contributor.authorTo, VSHen_HK
dc.date.accessioned2012-02-21T05:42:20Z-
dc.date.available2012-02-21T05:42:20Z-
dc.date.issued2011en_HK
dc.identifier.citationJournal Of Cancer Research And Clinical Oncology, 2011, v. 137 n. 3, p. 415-422en_HK
dc.identifier.issn0171-5216en_HK
dc.identifier.urihttp://hdl.handle.net/10722/145040-
dc.description.abstractAims: This study aimed at evaluating the potential anti-proliferative effects of the microRNA let-7 family in nasopharyngeal carcinoma (NPC) cells. In addition, the association between let-7 suppression and DNA hypermethylation is examined. Materials and methods: Levels of mature let-7 family members (-a,-b,-d,-e,-g, and-i) in normal nasopharyngeal cells (NP69 and NP460) and nasopharyngeal carcinoma cells (HK1 and HONE1) were measured by real-time quantitative PCR. Cell-proliferation assay and c-Myc immunohistochemical staining were performed on NPC cells transfected with let-7 precursor molecules. In addition, expression changes in let-7 family members in response to demethylating agents (5-azacytidine and zebularine) were also examined. Results: In comparison with the normal nasopharyngeal cells, let-7 (-a,-b,-d,-e,-g, and-i) levels were reduced in nasopharyngeal carcinoma cells. Ectopic expression of the let-7 family in nasopharyngeal carcinoma cells resulted in inhibition of cell proliferation through downregulation of c-Myc expression. Demethylation treatment of nasopharyngeal carcinoma cells caused activation of let-7 expression in poorly differentiated nasopharyngeal carcinoma cells only. Conclusion: Our results suggested that miRNA let-7 might play a role in the proliferation of NPC. DNA methylation is a potential regulatory pathway, which is affected when let-7 is suppressed in NPC cells. However, the extent of DNA hypermethylation/hypomethylation in regulating let-7 expression requires further elucidation. © The Author(s) 2010. This article is published with open access at Springerlink.com.en_HK
dc.languageengen_US
dc.publisherSpringer Verlag. The Journal's web site is located at http://link.springer.de/link/service/journals/00432/index.htmen_HK
dc.relation.ispartofJournal of Cancer Research and Clinical Oncologyen_HK
dc.rightsThe Author(s)en_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong Licenseen_US
dc.subjectEpigenetic regulationen_HK
dc.subjectLet-7en_HK
dc.subjectMicroRNAsen_HK
dc.subjectNasopharyngeal carcinomaen_HK
dc.subjectProliferationen_HK
dc.subject.meshCell Growth Processes - genetics-
dc.subject.meshGene Expression Regulation, Neoplastic-
dc.subject.meshMicroRNAs - genetics-
dc.subject.meshNasopharyngeal Neoplasms - genetics - metabolism - pathology-
dc.subject.meshProto-Oncogene Proteins c-myc - biosynthesis - genetics-
dc.titleMicroRNA let-7 suppresses nasopharyngeal carcinoma cells proliferation through downregulating c-Myc expressionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4551/resserv?sid=springerlink&genre=article&atitle=MicroRNA let-7 suppresses nasopharyngeal carcinoma cells proliferation through downregulating c-Myc expression&title=Journal of Cancer Research and Clinical Oncology&issn=01715216&date=2011-03-01&volume=137&issue=3& spage=415&authors=Thian-Sze Wong, On-Ying Man, Chi-Man Tsang, <i>et al.</i>en_US
dc.identifier.emailWong, TS: thiansze@graduate.hku.hken_HK
dc.identifier.emailTsao, SW: gswtsao@hkucc.hku.hken_HK
dc.identifier.emailTsang, RKY: rkytsang@hku.hken_HK
dc.identifier.emailChan, JYW: jywchan1@hku.hken_HK
dc.identifier.emailWei, WI: hrmswwi@hku.hken_HK
dc.identifier.emailTo, VSH: doctorto@hku.hken_HK
dc.identifier.authorityWong, TS=rp00478en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityTsang, RKY=rp01386en_HK
dc.identifier.authorityChan, JYW=rp01314en_HK
dc.identifier.authorityWei, WI=rp00323en_HK
dc.identifier.authorityTo, VSH=rp01385en_HK
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1007/s00432-010-0898-4en_HK
dc.identifier.pmid20440510-
dc.identifier.pmcidPMC3036828-
dc.identifier.scopuseid_2-s2.0-79954431152en_HK
dc.identifier.hkuros174116-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79954431152&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume137en_HK
dc.identifier.issue3en_HK
dc.identifier.spage415en_HK
dc.identifier.epage422en_HK
dc.identifier.eissn1432-1335en_US
dc.identifier.isiWOS:000287209200005-
dc.publisher.placeGermanyen_HK
dc.description.otherSpringer Open Choice, 21 Feb 2012en_US
dc.identifier.scopusauthoridWong, TS=7403531328en_HK
dc.identifier.scopusauthoridMan, OY=35956630500en_HK
dc.identifier.scopusauthoridTsang, CM=24831236400en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridTsang, RKY=7102940058en_HK
dc.identifier.scopusauthoridChan, JYW=27171772200en_HK
dc.identifier.scopusauthoridHo, WK=7402968844en_HK
dc.identifier.scopusauthoridWei, WI=7403321552en_HK
dc.identifier.scopusauthoridTo, VSH=35957345400en_HK
dc.identifier.citeulike7159732-

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