Cisplatin-induced senescence and growth inhibition in human non-small cell lung cancer cells with ectopic transfer of p16INK4a

Kang Fang, Chien Chih Chiu, Chin Hsiao Li, Yung Ta Chang, Hwei Tein Hwang

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19 Citations (Scopus)


DNA damage is lethal and capable of inducing cellular aging or apoptosis. In this work, the highly tumorigenic and cisplatin-resistant human non-small cell lung cancer (NSCLC) cells were transfected with construct encoding the complete sequence of p16INK4a (p16). The stable clones with elevated p16 exhibited enhanced sensitivities to low concentration cisplatin treatment. Further study indicated that cisplatin arrested cells at G2/M phase and the effectiveness is proportional to the level of p16 expressed. The growth of the xenograft tumors established by p16 transfectants in nude mice was also suppressed by cisplatin by inducing senescence-like phenotype. The data altogether indicated that, in cisplatin-resistant tumor cells with basal endogenous p16, the growth suppression by drugs can be greatly improved by ectopic gene transfer.

Original languageEnglish
Pages (from-to)479-488
Number of pages10
JournalOncology Research
Issue number10
Publication statusPublished - 2007 Dec 1



  • Cisplatin
  • Human non-small cell lung cancer cells
  • p16

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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