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Article: Mature miR-184 as potential oncogenic microRNA of squamous cell carcinoma of tongue

TitleMature miR-184 as potential oncogenic microRNA of squamous cell carcinoma of tongue
Authors
Issue Date2008
PublisherAmerican Association for Cancer Research.
Citation
Clinical Cancer Research, 2008, v. 14 n. 9, p. 2588-2592 How to Cite?
AbstractPurpose: The aim of this study was to evaluate the microRNA expression patterns in squamous cell carcinoma (SCC) of the tongue. Experimental Design: Expression levels of 156 human mature microRNAs were examined using real-time quantitative PCR (Taq Man MicroRNA Assays; Human Panel) on laser microdis-sected cells of 4 tongue carcinomas and paired normal tissues. Expression of mature miR-184 was further validated in 20 paired tongue SCC and the normal tissues. Potential oncogenic functions of miR-184 were evaluated in tongue SCC cell lines (Cal27, HN21B, and HN96) with miR-184 inhibitor. Plasma miR-184 levels were evaluated using real-time quantitative PCR. Results: Using 3-fold expression difference as a cutoff level, we identified 24 up-regulated mature miRNAs including miR-184, miR-34c, miR-137, miR-372, miR-124a, miR-21, miR-124b, miR-31, miR-128a, miR-34b, miR-154, miR-197, miR-132, miR-147, miR-325, miR-181c, miR-198, miR-155, miR-30a-3p, miR-338, miR-17-5p, miR-104, miR-134, and miR-213; and 13 down-regulated mature miRNAs including miR-133a, miR-99a, miR-194, miR-133b, miR-219, miR-100, miR-125b, miR-26b, miR-138, miR-149, miR-195, miR-107, and miR-139. Overexpres-sion of miR-184 was further validated in 20 paired tongue SCC and normal tissues (P = 0.002). Inhibition of miR-184 in tongue SCC cell lines could reduce cell proliferation rate. Down-regulation of c-Myc was observed in two cell lines in response to miR-184 inhibitor. Suppressing miR-184 could induce apoptosis in all three cell lines. Plasma miR-184 levels were significantly higher in tongue SCC patients in comparison with normal individuals, and the levels were significantly reduced after surgical removal of the primary tumors. Conclusions: Overexpression of miR-184 might play an oncogenic role in the antiapoptotic and proliferative processes of tongue SCC. In addition, plasma miR-184 levels were associated with the presence of primary tumor. Further studies on the aberrantly expressed miRNAs in tongue SCC as well as using plasma miRNAs as novel tumor markers are warranted. © 2008 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/83279
ISSN
2015 Impact Factor: 8.738
2015 SCImago Journal Rankings: 5.314
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, TSen_HK
dc.contributor.authorLiu, XBen_HK
dc.contributor.authorWong, BYHen_HK
dc.contributor.authorNg, RWMen_HK
dc.contributor.authorYuen, APWen_HK
dc.contributor.authorWei, WIen_HK
dc.date.accessioned2010-09-06T08:39:08Z-
dc.date.available2010-09-06T08:39:08Z-
dc.date.issued2008en_HK
dc.identifier.citationClinical Cancer Research, 2008, v. 14 n. 9, p. 2588-2592en_HK
dc.identifier.issn1078-0432en_HK
dc.identifier.urihttp://hdl.handle.net/10722/83279-
dc.description.abstractPurpose: The aim of this study was to evaluate the microRNA expression patterns in squamous cell carcinoma (SCC) of the tongue. Experimental Design: Expression levels of 156 human mature microRNAs were examined using real-time quantitative PCR (Taq Man MicroRNA Assays; Human Panel) on laser microdis-sected cells of 4 tongue carcinomas and paired normal tissues. Expression of mature miR-184 was further validated in 20 paired tongue SCC and the normal tissues. Potential oncogenic functions of miR-184 were evaluated in tongue SCC cell lines (Cal27, HN21B, and HN96) with miR-184 inhibitor. Plasma miR-184 levels were evaluated using real-time quantitative PCR. Results: Using 3-fold expression difference as a cutoff level, we identified 24 up-regulated mature miRNAs including miR-184, miR-34c, miR-137, miR-372, miR-124a, miR-21, miR-124b, miR-31, miR-128a, miR-34b, miR-154, miR-197, miR-132, miR-147, miR-325, miR-181c, miR-198, miR-155, miR-30a-3p, miR-338, miR-17-5p, miR-104, miR-134, and miR-213; and 13 down-regulated mature miRNAs including miR-133a, miR-99a, miR-194, miR-133b, miR-219, miR-100, miR-125b, miR-26b, miR-138, miR-149, miR-195, miR-107, and miR-139. Overexpres-sion of miR-184 was further validated in 20 paired tongue SCC and normal tissues (P = 0.002). Inhibition of miR-184 in tongue SCC cell lines could reduce cell proliferation rate. Down-regulation of c-Myc was observed in two cell lines in response to miR-184 inhibitor. Suppressing miR-184 could induce apoptosis in all three cell lines. Plasma miR-184 levels were significantly higher in tongue SCC patients in comparison with normal individuals, and the levels were significantly reduced after surgical removal of the primary tumors. Conclusions: Overexpression of miR-184 might play an oncogenic role in the antiapoptotic and proliferative processes of tongue SCC. In addition, plasma miR-184 levels were associated with the presence of primary tumor. Further studies on the aberrantly expressed miRNAs in tongue SCC as well as using plasma miRNAs as novel tumor markers are warranted. © 2008 American Association for Cancer Research.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research.en_HK
dc.relation.ispartofClinical Cancer Researchen_HK
dc.subject.meshCarcinoma, Squamous Cell - metabolism-
dc.subject.meshCell Line, Tumor-
dc.subject.meshMicroRNAs - antagonists and inhibitors - blood - metabolism-
dc.subject.meshProto-Oncogene Proteins c-myc - metabolism-
dc.subject.meshTongue Neoplasms - metabolism-
dc.titleMature miR-184 as potential oncogenic microRNA of squamous cell carcinoma of tongueen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1078-0432&volume=14&issue=9&spage=2588&epage=2592&date=2008&atitle=Mature+miR-184+as+potential+oncogenic+miRNA+in+squamous+cell+carcinoma+of+tongue+en_HK
dc.identifier.emailWong, TS: thiansze@graduate.hku.hken_HK
dc.identifier.emailWei, WI: hrmswwi@hku.hken_HK
dc.identifier.authorityWong, TS=rp00478en_HK
dc.identifier.authorityWei, WI=rp00323en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1158/1078-0432.CCR-07-0666en_HK
dc.identifier.pmid18451220-
dc.identifier.scopuseid_2-s2.0-52049121293en_HK
dc.identifier.hkuros162261en_HK
dc.identifier.hkuros142451-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-52049121293&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume14en_HK
dc.identifier.issue9en_HK
dc.identifier.spage2588en_HK
dc.identifier.epage2592en_HK
dc.identifier.eissn1557-3265-
dc.identifier.isiWOS:000255616300009-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, TS=7403531328en_HK
dc.identifier.scopusauthoridLiu, XB=26642902000en_HK
dc.identifier.scopusauthoridWong, BYH=7402023295en_HK
dc.identifier.scopusauthoridNg, RWM=7102153861en_HK
dc.identifier.scopusauthoridYuen, APW=7006290111en_HK
dc.identifier.scopusauthoridWei, WI=7403321552en_HK
dc.identifier.citeulike3859572-

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