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

Oncology Research
Kang FangHwei-tein Hwang

Abstract

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.

Citations

Jan 28, 2009·Apoptosis : an International Journal on Programmed Cell Death·Hagit GrimbergIlan Ziv
Oct 1, 2009·Epigenomics·Francesco CreaWilliam L Farrar
Aug 16, 2019·Cellular and Molecular Life Sciences : CMLS·Justyna Mikuła-PietrasikKrzysztof Książek
Sep 16, 2016·Aging Cell·Nadezhda V PetrovaOmar L Kantidze
Apr 3, 2020·International Journal of Oncology·Alice ZamagniChiara Molinari
Jul 2, 2019·Seminars in Cancer Biology·Eleni MavrogonatouDimitris Kletsas
Jun 23, 2010·Journal of Experimental & Clinical Cancer Research : CR·Wei ZhangSongbin Fu

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