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

Research output: Contribution to journalArticle

18 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)479-488
Number of pages10
JournalOncology Research
Volume16
Issue number10
DOIs
Publication statusPublished - 2007 Dec 1

Fingerprint

Non-Small Cell Lung Carcinoma
Cisplatin
Growth
Cell Aging
G2 Phase
Heterografts
Nude Mice
Cell Division
DNA Damage
Neoplasms
Clone Cells
Apoptosis
Phenotype
Pharmaceutical Preparations
Genes

Keywords

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

ASJC Scopus subject areas

  • Cancer Research

Cite this

Cisplatin-induced senescence and growth inhibition in human non-small cell lung cancer cells with ectopic transfer of p16INK4a . / Fang, Kang; Chiu, Chien Chih; Li, Chin Hsiao; Chang, Yung-Ta; Hwang, Hwei Tein.

In: Oncology Research, Vol. 16, No. 10, 01.12.2007, p. 479-488.

Research output: Contribution to journalArticle

@article{3f17646c6065493e81b4e7b012b8054f,
title = "Cisplatin-induced senescence and growth inhibition in human non-small cell lung cancer cells with ectopic transfer of p16INK4a",
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.",
keywords = "Cisplatin, Human non-small cell lung cancer cells, p16",
author = "Kang Fang and Chiu, {Chien Chih} and Li, {Chin Hsiao} and Yung-Ta Chang and Hwang, {Hwei Tein}",
year = "2007",
month = "12",
day = "1",
doi = "10.3727/096504007783338331",
language = "English",
volume = "16",
pages = "479--488",
journal = "Oncology Research",
issn = "0965-0407",
publisher = "Cognizant Communication Corporation",
number = "10",

}

TY - JOUR

T1 - Cisplatin-induced senescence and growth inhibition in human non-small cell lung cancer cells with ectopic transfer of p16INK4a

AU - Fang, Kang

AU - Chiu, Chien Chih

AU - Li, Chin Hsiao

AU - Chang, Yung-Ta

AU - Hwang, Hwei Tein

PY - 2007/12/1

Y1 - 2007/12/1

N2 - 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.

AB - 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.

KW - Cisplatin

KW - Human non-small cell lung cancer cells

KW - p16

UR - http://www.scopus.com/inward/record.url?scp=38149024065&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=38149024065&partnerID=8YFLogxK

U2 - 10.3727/096504007783338331

DO - 10.3727/096504007783338331

M3 - Article

C2 - 18196872

AN - SCOPUS:38149024065

VL - 16

SP - 479

EP - 488

JO - Oncology Research

JF - Oncology Research

SN - 0965-0407

IS - 10

ER -