Inhibiting tumorigenic potential by restoration of p16 in nasopharyngeal carcinoma
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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, (C) 1999 Cancer Research Campaign.
All Author(s) ListWang GL, Lo KW, Tsang KS, Chung NYF, Tsang YS, Cheung ST, Lee JCK, Huang DP
Journal nameBritish Journal of Cancer
Year1999
Month12
Day1
Volume Number81
Issue Number7
PublisherCHURCHILL LIVINGSTONE
Pages1122 - 1126
ISSN0007-0920
eISSN1532-1827
LanguagesEnglish-United Kingdom
Keywordsgene transfer; nasopharyngeal carcinoma; p16; tumour suppressor
Web of Science Subject CategoriesOncology; ONCOLOGY

Last updated on 2020-26-10 at 01:25