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Article: Metastasis-suppressing NID2, an epigenetically silenced gene, in the pathologenesis of nasopharyngeal carcinoma and esophageal squamous cell carcinoma

TitleMetastasis-suppressing NID2, an epigenetically silenced gene, in the pathologenesis of nasopharyngeal carcinoma and esophageal squamous cell carcinoma
Authors
KeywordsEsophageal squamous cell carcinoma (ESCC)
Metastasis
Nasopharyngeal carcinoma (NPC)
Nidogen-2 (NID2)
Promoter hypermethylation
Issue Date2016
PublisherImpact Journals LLC. The Journal's web site is located at http://www.impactjournals.com/oncotarget/index.html
Citation
Oncotarget, 2016, v. 7 n. 48, p. 78859-78871 How to Cite?
AbstractNidogen-2 (NID2) is a key component of the basement membrane that stabilizes the extracellular matrix (ECM) network. The aim of the study is to analyze the functional roles of NID2 in the pathogenesis of nasopharyngeal carcinoma (NPC) and esophageal squamous cell carcinoma (ESCC). We performed genome-wide methylation profiling of NPC and ESCC and validated our findings using the methylation-sensitive high-resolution melting (MS-HRM) assay. Results showed that promoter methylation of NID2 was significantly higher in NPC and ESCC samples than in their adjacent non-cancer counterparts. Consistently, down-regulation of NID2 was observed in the clinical samples and cell lines of both NPC and ESCC. Re-expression of NID2 suppresses clonogenic survival and migration abilities of transduced NPC and ESCC cells. We showed that NID2 significantly inhibits liver metastasis. Mechanistic studies of signaling pathways also confirm that NID2 suppresses the EGFR/Akt and integrin/ FAK/PLCγ metastasis-related pathways. This study provides novel insights into the crucial tumor metastasis suppression roles of NID2 in cancers.
Persistent Identifierhttp://hdl.handle.net/10722/243064
ISSN
2015 Impact Factor: 5.008
2015 SCImago Journal Rankings: 2.294
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorCHAI, WY-
dc.contributor.authorCheung, AKL-
dc.contributor.authorDai, W-
dc.contributor.authorKo, JMY-
dc.contributor.authorIp, JCY-
dc.contributor.authorChan, KW-
dc.contributor.authorKwong, DLW-
dc.contributor.authorNg, WT-
dc.contributor.authorLee, WMA-
dc.contributor.authorNgan, KC-
dc.contributor.authorYau, CC-
dc.contributor.authorTung, SY-
dc.contributor.authorLee, VHF-
dc.contributor.authorLam, AKY-
dc.contributor.authorPillai, S-
dc.contributor.authorLaw, SYK-
dc.contributor.authorLung, ML-
dc.date.accessioned2017-08-25T02:49:27Z-
dc.date.available2017-08-25T02:49:27Z-
dc.date.issued2016-
dc.identifier.citationOncotarget, 2016, v. 7 n. 48, p. 78859-78871-
dc.identifier.issn1949-2553-
dc.identifier.urihttp://hdl.handle.net/10722/243064-
dc.description.abstractNidogen-2 (NID2) is a key component of the basement membrane that stabilizes the extracellular matrix (ECM) network. The aim of the study is to analyze the functional roles of NID2 in the pathogenesis of nasopharyngeal carcinoma (NPC) and esophageal squamous cell carcinoma (ESCC). We performed genome-wide methylation profiling of NPC and ESCC and validated our findings using the methylation-sensitive high-resolution melting (MS-HRM) assay. Results showed that promoter methylation of NID2 was significantly higher in NPC and ESCC samples than in their adjacent non-cancer counterparts. Consistently, down-regulation of NID2 was observed in the clinical samples and cell lines of both NPC and ESCC. Re-expression of NID2 suppresses clonogenic survival and migration abilities of transduced NPC and ESCC cells. We showed that NID2 significantly inhibits liver metastasis. Mechanistic studies of signaling pathways also confirm that NID2 suppresses the EGFR/Akt and integrin/ FAK/PLCγ metastasis-related pathways. This study provides novel insights into the crucial tumor metastasis suppression roles of NID2 in cancers.-
dc.languageeng-
dc.publisherImpact Journals LLC. The Journal's web site is located at http://www.impactjournals.com/oncotarget/index.html-
dc.relation.ispartofOncotarget-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectEsophageal squamous cell carcinoma (ESCC)-
dc.subjectMetastasis-
dc.subjectNasopharyngeal carcinoma (NPC)-
dc.subjectNidogen-2 (NID2)-
dc.subjectPromoter hypermethylation-
dc.titleMetastasis-suppressing NID2, an epigenetically silenced gene, in the pathologenesis of nasopharyngeal carcinoma and esophageal squamous cell carcinoma-
dc.typeArticle-
dc.identifier.emailCheung, AKL: arthurhk@hku.hk-
dc.identifier.emailDai, W: weidai2@hku.hk-
dc.identifier.emailKo, JMY: joko@hku.hk-
dc.identifier.emailIp, JCY: josephip@hku.hk-
dc.identifier.emailChan, KW: kwchan@pathology.hku.hk-
dc.identifier.emailKwong, DLW: dlwkwong@hku.hk-
dc.identifier.emailNg, WT: ngwt1@hkucc.hku.hk-
dc.identifier.emailLee, WMA: awmlee@hkucc.hku.hk-
dc.identifier.emailNgan, KC: rkcngan@hkucc.hku.hk-
dc.identifier.emailLee, VHF: vhflee@hku.hk-
dc.identifier.emailLaw, SYK: slaw@hkucc.hku.hk-
dc.identifier.emailLung, ML: mlilung@hku.hk-
dc.identifier.authorityCheung, AKL=rp01769-
dc.identifier.authorityDai, W=rp02146-
dc.identifier.authorityKo, JMY=rp02011-
dc.identifier.authorityChan, KW=rp00330-
dc.identifier.authorityKwong, DLW=rp00414-
dc.identifier.authorityLee, WMA=rp02056-
dc.identifier.authorityLee, VHF=rp00264-
dc.identifier.authorityLaw, SYK=rp00437-
dc.identifier.authorityLung, ML=rp00300-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.18632/oncotarget.12889-
dc.identifier.pmid27793011-
dc.identifier.pmcidPMC5346683-
dc.identifier.scopuseid_2-s2.0-84999836729-
dc.identifier.hkuros274516-
dc.identifier.hkuros271610-
dc.identifier.volume7-
dc.identifier.issue48-
dc.identifier.spage78859-
dc.identifier.epage78871-
dc.publisher.placeUnited States-

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