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Article: MicroRNA-144 promotes cell proliferation, migration and invasion in nasopharyngeal carcinoma through repression of PTEN

TitleMicroRNA-144 promotes cell proliferation, migration and invasion in nasopharyngeal carcinoma through repression of PTEN
Authors
Issue Date2013
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2013, v. 34 n. 2, p. 454-463 How to Cite?
AbstractNasopharyngeal carcinoma (NPC) is a type of head and neck cancer with significantly high prevalence in Southern China. Unlike other head and neck cancers, mutations or deletions of tumor suppressor genes in NPC are not common. Recently, downregulation of tumor suppressor genes expression by microRNA (miRNA) is increasingly recognized as an important mechanism of nasopharyngeal tumorigenesis. In this study, we reported that microRNA-144 (miR-144) was frequently upregulated in NPC specimens and cell lines. Repression of miR-144 significantly decreased cell proliferation, clonogenicity, migration, invasion and tumor formation in nude mice, while restoring miR-144 in miR-144-attenuated NPC cells exhibited a strong tumorigenic role. Further, we found that miR-144 was inversely correlated with the tumor suppressor gene phosphatase and tensin homolog (PTEN) in NPC specimens and cell lines, and then we identified PTEN as a direct target of miR-144 in NPC cell lines. PTEN downregulation in miR-144-attenuated cells could increase cell growth, migration and invasion. Mechanistic investigations revealed that miR-144 suppressed the expression of PTEN to increase the expression of pAkt and cyclin D1 to promote G1-phase transition and decrease E-cadherin to promote migration and invasion. Taken together, we provide compelling evidence that miR-144 functions as an onco-miRNA in NPC, and its oncoeffects are mediated chiefly by repressing PTEN expression to activate the PI3K/Akt pathway. © Crown copyright 2012.
Persistent Identifierhttp://hdl.handle.net/10722/185623
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.439
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZHANG, L-
dc.contributor.authorLee, VHF-
dc.contributor.authorWONG, AMG-
dc.contributor.authorZhu, Y-
dc.contributor.authorDong, S-
dc.contributor.authorKONG, KL-
dc.contributor.authorCHEN, J-
dc.contributor.authorTsao, GSW-
dc.contributor.authorGuan, X-
dc.contributor.authorFu, L-
dc.date.accessioned2013-08-20T11:34:41Z-
dc.date.available2013-08-20T11:34:41Z-
dc.date.issued2013-
dc.identifier.citationCarcinogenesis, 2013, v. 34 n. 2, p. 454-463-
dc.identifier.issn0143-3334-
dc.identifier.urihttp://hdl.handle.net/10722/185623-
dc.description.abstractNasopharyngeal carcinoma (NPC) is a type of head and neck cancer with significantly high prevalence in Southern China. Unlike other head and neck cancers, mutations or deletions of tumor suppressor genes in NPC are not common. Recently, downregulation of tumor suppressor genes expression by microRNA (miRNA) is increasingly recognized as an important mechanism of nasopharyngeal tumorigenesis. In this study, we reported that microRNA-144 (miR-144) was frequently upregulated in NPC specimens and cell lines. Repression of miR-144 significantly decreased cell proliferation, clonogenicity, migration, invasion and tumor formation in nude mice, while restoring miR-144 in miR-144-attenuated NPC cells exhibited a strong tumorigenic role. Further, we found that miR-144 was inversely correlated with the tumor suppressor gene phosphatase and tensin homolog (PTEN) in NPC specimens and cell lines, and then we identified PTEN as a direct target of miR-144 in NPC cell lines. PTEN downregulation in miR-144-attenuated cells could increase cell growth, migration and invasion. Mechanistic investigations revealed that miR-144 suppressed the expression of PTEN to increase the expression of pAkt and cyclin D1 to promote G1-phase transition and decrease E-cadherin to promote migration and invasion. Taken together, we provide compelling evidence that miR-144 functions as an onco-miRNA in NPC, and its oncoeffects are mediated chiefly by repressing PTEN expression to activate the PI3K/Akt pathway. © Crown copyright 2012.-
dc.languageeng-
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/-
dc.relation.ispartofCarcinogenesis-
dc.rightsPre-print: Journal Title] ©: [year] [owner as specified on the article] Published by Oxford University Press [on behalf of xxxxxx]. All rights reserved. Pre-print (Once an article is published, preprint notice should be amended to): This is an electronic version of an article published in [include the complete citation information for the final version of the Article as published in the print edition of the Journal.] Post-print: This is a pre-copy-editing, author-produced PDF of an article accepted for publication in [insert journal title] following peer review. The definitive publisher-authenticated version [insert complete citation information here] is available online at: xxxxxxx [insert URL that the author will receive upon publication here].-
dc.titleMicroRNA-144 promotes cell proliferation, migration and invasion in nasopharyngeal carcinoma through repression of PTEN-
dc.typeArticle-
dc.identifier.emailLee, VHF: vhflee@hku.hk-
dc.identifier.emailDong, S: dongss@hku.hk-
dc.identifier.emailTsao, GSW: gswtsao@hku.hk-
dc.identifier.emailGuan, X: xyguan@hkucc.hku.hk-
dc.identifier.emailFu, L: gracefu@graduate.hku.hk-
dc.identifier.authorityLee, VHF=rp00264-
dc.identifier.authorityTsao, GSW=rp00399-
dc.identifier.authorityGuan, X=rp00454-
dc.identifier.authorityFu, L=rp01435-
dc.identifier.doi10.1093/carcin/bgs346-
dc.identifier.pmid23125220-
dc.identifier.scopuseid_2-s2.0-84873542829-
dc.identifier.hkuros218260-
dc.identifier.volume34-
dc.identifier.issue2-
dc.identifier.spage454-
dc.identifier.epage463-
dc.identifier.isiWOS:000315627900026-
dc.publisher.placeUnited Kingdom-

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