The suppressed proliferation and premature senescence by ganciclovir in p53-mutated human non-small-lung cancer cells acquiring herpes simplex virus-thymidine kinase cDNA

C. C. Chiu, C. H. Li, T. S. Fuh, W. L. Chen, C. S. Huang, L. J. Chen, W. H. Ung, K. Fang

Research output: Contribution to journalArticle

8 Citations (Scopus)


The concerted actions of molecular networks determine how cells undergo proliferation, death or aging. Here we show that the highly invasive, tumorigenic human non-small-cell-lung cancer (NSCLC) cells carrying mutated p53 alleles were transfected with herpes simplex virus-thymidine kinase (HSV-tk) cDNA and the selected clone was susceptible to exogenous ganciclovir (GCV). The work further indicated that, in the stable HSV-tk transfectants, GCV suppressed cell proliferation by inducing G2/M cell cycle arrest and premature senescence and the potency can be amplified through bystander effect. The growth suppression of the established tumor xenografts in nude mice can be successfully targeted by GCV. These data showed that the GCV-suppressed tumor cell proliferation can be coordinated by cell cycle arrest and cellular senescence in HSV-tk transfectant lacking wild-type p53.

Original languageEnglish
Pages (from-to)286-293
Number of pages8
JournalCancer Detection and Prevention
Issue number3
Publication statusPublished - 2005 Jun 17



  • Herpes simplex virus-thymidine kinase
  • Human non-small-cell-lung cancer cells

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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