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Article: Proteomic profiling between CNE-2 and its strongly metastatic subclone S-18 and functional characterization of HSP27 in metastasis of nasopharyngeal carcinoma

TitleProteomic profiling between CNE-2 and its strongly metastatic subclone S-18 and functional characterization of HSP27 in metastasis of nasopharyngeal carcinoma
Authors
Issue Date2011
PublisherWiley - V C H Verlag GmbH & Co KGaA. The Journal's web site is located at http://www.wiley-vch.de/home/proteomics
Citation
Proteomics, 2011, v. 11 n. 14, p. 2911-2920 How to Cite?
AbstractMetastasis to secondary sites remains the leading cause of nasopharyngeal carcinoma (NPC)-associated death. In order to identify the candidate protein(s) responsible for the differential metastatic capacity, the protein expression profiling between NPC cell line CNE-2 and its highly metastatic subclone S-18 were compared by 2-DE. In total, 18 spots were differentially expressed between these two cell lines. Among all, seven proteins were identified with further MS analysis. Western blotting further validated upregulation of HSP27 and ezrin, and downregulation of valosin containing protein and keratin 18 in S-18. Moreover, the knockdown of HSP27 was found to significantly decrease the invasive ability of S-18. On the other hand, overexpression of HSP27 in NP460 cells, which generated little endogenous HSP27 and less invasive, was noted to gain enhanced metastatic capability. Real-time PCR confirmed that the transcriptional levels of NF-κB and MMP9, MMP11 were downregulated after inhibition of HSP27 in S-18, which implicated that HSP27 enhanced the metastatic property of NPC cells probably via the NF-κB-mediated activation of MMPs. The findings in this work provided us a platform for further elucidating the underlying mechanisms of NPC metastasis and demonstrated that HSP27 would be a valid target for anti-cancer drug development. © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
Persistent Identifierhttp://hdl.handle.net/10722/168536
ISSN
2015 Impact Factor: 4.079
2015 SCImago Journal Rankings: 1.476
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, GPen_US
dc.contributor.authorWang, Hen_US
dc.contributor.authorLai, YKen_US
dc.contributor.authorChen, SCen_US
dc.contributor.authorLin, MCMen_US
dc.contributor.authorLu, Gen_US
dc.contributor.authorZhang, JFen_US
dc.contributor.authorHe, XGen_US
dc.contributor.authorQian, CNen_US
dc.contributor.authorKung, HFen_US
dc.date.accessioned2012-10-08T03:20:14Z-
dc.date.available2012-10-08T03:20:14Z-
dc.date.issued2011en_US
dc.identifier.citationProteomics, 2011, v. 11 n. 14, p. 2911-2920en_US
dc.identifier.issn1615-9853en_US
dc.identifier.urihttp://hdl.handle.net/10722/168536-
dc.description.abstractMetastasis to secondary sites remains the leading cause of nasopharyngeal carcinoma (NPC)-associated death. In order to identify the candidate protein(s) responsible for the differential metastatic capacity, the protein expression profiling between NPC cell line CNE-2 and its highly metastatic subclone S-18 were compared by 2-DE. In total, 18 spots were differentially expressed between these two cell lines. Among all, seven proteins were identified with further MS analysis. Western blotting further validated upregulation of HSP27 and ezrin, and downregulation of valosin containing protein and keratin 18 in S-18. Moreover, the knockdown of HSP27 was found to significantly decrease the invasive ability of S-18. On the other hand, overexpression of HSP27 in NP460 cells, which generated little endogenous HSP27 and less invasive, was noted to gain enhanced metastatic capability. Real-time PCR confirmed that the transcriptional levels of NF-κB and MMP9, MMP11 were downregulated after inhibition of HSP27 in S-18, which implicated that HSP27 enhanced the metastatic property of NPC cells probably via the NF-κB-mediated activation of MMPs. The findings in this work provided us a platform for further elucidating the underlying mechanisms of NPC metastasis and demonstrated that HSP27 would be a valid target for anti-cancer drug development. © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.en_US
dc.languageengen_US
dc.publisherWiley - V C H Verlag GmbH & Co KGaA. The Journal's web site is located at http://www.wiley-vch.de/home/proteomicsen_US
dc.relation.ispartofProteomicsen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshElectrophoresis, Gel, Two-Dimensional - Methodsen_US
dc.subject.meshHsp27 Heat-Shock Proteins - Chemistry - Genetics - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshMass Spectrometry - Methodsen_US
dc.subject.meshMatrix Metalloproteinases - Genetics - Metabolismen_US
dc.subject.meshNf-Kappa B - Metabolismen_US
dc.subject.meshNasopharyngeal Neoplasms - Pathologyen_US
dc.subject.meshNeoplasm Metastasisen_US
dc.subject.meshNeoplasm Proteins - Chemistry - Genetics - Metabolismen_US
dc.subject.meshProteome - Analysisen_US
dc.subject.meshProteomics - Methodsen_US
dc.subject.meshRna, Small Interfering - Genetics - Metabolismen_US
dc.titleProteomic profiling between CNE-2 and its strongly metastatic subclone S-18 and functional characterization of HSP27 in metastasis of nasopharyngeal carcinomaen_US
dc.typeArticleen_US
dc.identifier.emailLin, MCM:mcllin@hkucc.hku.hken_US
dc.identifier.authorityLin, MCM=rp00746en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1002/pmic.201000483en_US
dc.identifier.pmid21717573-
dc.identifier.scopuseid_2-s2.0-79959769116en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79959769116&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume11en_US
dc.identifier.issue14en_US
dc.identifier.spage2911en_US
dc.identifier.epage2920en_US
dc.identifier.isiWOS:000293268100014-
dc.publisher.placeGermanyen_US
dc.identifier.scopusauthoridLi, GP=54781550300en_US
dc.identifier.scopusauthoridWang, H=7501747965en_US
dc.identifier.scopusauthoridLai, YK=7401512434en_US
dc.identifier.scopusauthoridChen, SC=35092110300en_US
dc.identifier.scopusauthoridLin, MCM=7404816359en_US
dc.identifier.scopusauthoridLu, G=36619108300en_US
dc.identifier.scopusauthoridZhang, JF=54781915000en_US
dc.identifier.scopusauthoridHe, XG=54781371700en_US
dc.identifier.scopusauthoridQian, CN=7202311133en_US
dc.identifier.scopusauthoridKung, HF=7402514190en_US

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