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Article: Inhibiting tumorigenic potential by restoration of p16 in nasopharyngeal carcinoma

TitleInhibiting tumorigenic potential by restoration of p16 in nasopharyngeal carcinoma
Authors
KeywordsGene transfer
Nasopharyngeal carcinoma
p16
Tumour suppressor
Issue Date1999
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjc
Citation
British Journal Of Cancer, 1999, v. 81 n. 7, p. 1122-1126 How to Cite?
AbstractThe p16 gene, encodes a key checkpoint protein p16 in the cell cycle, has been reported inactivation in a wide variety of human cancers. We have previously demonstrated high frequency of p16 alterations in primary nasopharyngeal carcinoma (NPC), xenografts and cell lines. The finding implied that inactivation of the p16 gene may play an important role in the NPC development. To investigate the tumour suppressor function of p16 in NPC, we tranfected p16-deficient NPC cell line, NPC/HK-1, with a wild-type p16 expression construct, and evaluated growth and tumorigenic properties of the clones stably expressing exogenous p16. Expression of the exogenous wild-type p16 significantly inhibited cell growth by more than 70% when compared to that of the parental and empty vector-transfected cells. This growth inhibition was attributable to a significant proportion of p16-expressing cells arrested at G1 phase in the cell cycle as revealed by flow cytometric analysis. By anchorage-independent colony forming assay, we found that the ability to form colonies in soft agar was highly reduced in cells expressing p16. NPC/HK1 cells expressing functional p16 also showed suppressed tumorigenicity in athymic nude mice. Taken together, our results provide strong evidence for a tumour suppressor role of p16 in NPC.
Persistent Identifierhttp://hdl.handle.net/10722/84110
ISSN
2015 Impact Factor: 5.569
2015 SCImago Journal Rankings: 2.939
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, GLen_HK
dc.contributor.authorLo, KWen_HK
dc.contributor.authorTsang, KSen_HK
dc.contributor.authorChung, NYFen_HK
dc.contributor.authorTsang, YSen_HK
dc.contributor.authorCheung, STen_HK
dc.contributor.authorLee, JCKen_HK
dc.contributor.authorHuang, DPen_HK
dc.date.accessioned2010-09-06T08:49:03Z-
dc.date.available2010-09-06T08:49:03Z-
dc.date.issued1999en_HK
dc.identifier.citationBritish Journal Of Cancer, 1999, v. 81 n. 7, p. 1122-1126en_HK
dc.identifier.issn0007-0920en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84110-
dc.description.abstractThe p16 gene, encodes a key checkpoint protein p16 in the cell cycle, has been reported inactivation in a wide variety of human cancers. We have previously demonstrated high frequency of p16 alterations in primary nasopharyngeal carcinoma (NPC), xenografts and cell lines. The finding implied that inactivation of the p16 gene may play an important role in the NPC development. To investigate the tumour suppressor function of p16 in NPC, we tranfected p16-deficient NPC cell line, NPC/HK-1, with a wild-type p16 expression construct, and evaluated growth and tumorigenic properties of the clones stably expressing exogenous p16. Expression of the exogenous wild-type p16 significantly inhibited cell growth by more than 70% when compared to that of the parental and empty vector-transfected cells. This growth inhibition was attributable to a significant proportion of p16-expressing cells arrested at G1 phase in the cell cycle as revealed by flow cytometric analysis. By anchorage-independent colony forming assay, we found that the ability to form colonies in soft agar was highly reduced in cells expressing p16. NPC/HK1 cells expressing functional p16 also showed suppressed tumorigenicity in athymic nude mice. Taken together, our results provide strong evidence for a tumour suppressor role of p16 in NPC.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjcen_HK
dc.relation.ispartofBritish Journal of Canceren_HK
dc.subjectGene transferen_HK
dc.subjectNasopharyngeal carcinomaen_HK
dc.subjectp16en_HK
dc.subjectTumour suppressoren_HK
dc.titleInhibiting tumorigenic potential by restoration of p16 in nasopharyngeal carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-0920&volume=81&spage=1122&epage=1126&date=1999&atitle=Inhibiting+tumorigenic+potential+by+restoration+of+p16+in+nasopharyngeal+carcinomaen_HK
dc.identifier.emailCheung, ST: stcheung@hkucc.hku.hken_HK
dc.identifier.authorityCheung, ST=rp00457en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid10584871-
dc.identifier.scopuseid_2-s2.0-0032759897en_HK
dc.identifier.hkuros51625en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032759897&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume81en_HK
dc.identifier.issue7en_HK
dc.identifier.spage1122en_HK
dc.identifier.epage1126en_HK
dc.identifier.isiWOS:000083774900006-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridWang, GL=21433827500en_HK
dc.identifier.scopusauthoridLo, KW=7402101603en_HK
dc.identifier.scopusauthoridTsang, KS=7201555004en_HK
dc.identifier.scopusauthoridChung, NYF=8868158900en_HK
dc.identifier.scopusauthoridTsang, YS=7007101172en_HK
dc.identifier.scopusauthoridCheung, ST=7202473497en_HK
dc.identifier.scopusauthoridLee, JCK=7601456915en_HK
dc.identifier.scopusauthoridHuang, DP=7403891486en_HK

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