Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1997 Jan;88(1):39-43.
doi: 10.1111/j.1349-7006.1997.tb00299.x.

Induction of p53-independent apoptosis associated with G2M arrest following DNA damage in human colon cancer cell lines

D Arita  1 , M Kambe, C Ishioka, R Kanamaru
Affiliations

Induction of p53-independent apoptosis associated with G2M arrest following DNA damage in human colon cancer cell lines

D Arita et al. Jpn J Cancer Res. 1997 Jan.

Abstract

The tumor suppressor p53 protein induces apoptosis in response to various kinds of DNA damage in normal cells, but it is still unclear whether or not apoptosis induced by DNA damage correlates with the p53 status in tumor cells. We determined the status of p53 by functional analysis of separated alleles in yeast in five human colon cancer cell lines, SW-480, SW-620, DLD-1, COLO320 and LS174T and investigated whether p53 is necessary for apoptosis and cell cycle arrest after treatment of the cells with a DNA-damaging agent, etoposide (VP-16), or gamma-irradiation. Of these cell lines, only LS174T expresses a functional p53. Apoptosis was detected in SW-480 and COLO320 cell lines, but not in the other cell lines, including LS174T cell line with a normal p53 function. Furthermore, cell cycle analysis revealed accumulation in the G2M phase preceding induction of apoptosis in SW-480 and COLO320 cells, but not in the other cells. These results suggest that apoptotic induction by DNA damage is not necessarily related to p53 status and that induction of p53-independent apoptosis following DNA damage may correlate with G2M arrest in the cell cycle, at least in the colon cancer cell lines used in this study.

PubMed Disclaimer

References

    1. ) Kerr , J. F. R. , Wyllie , A. H. and Currie , A. R.Apoptosis: a basic biological phenomenon with wide ranging implications in tissue kinetics . Br. J. Cancer , 26239 – 257 ( 1972. ). - PMC - PubMed
    1. ) Wyllie , A. H. , Morris , R. G. and Dunlop , D.Chromatin cleavage in apoptosis: association with condensed chromatin morphology and dependence on macromolecular synthesis . J. Pathol , 142 , 67 – 77 ( 1984. ). - PubMed
    1. ) Yoshida , A. , Ueda , T. , Takauji , R. , Liu , Y. , Fukushima , M. and Nakamura , T.Role of calcium ion in induction of apoptosis by etoposide in human HL‐60 cells . Biochem. Siophys. Res. Commun , 196 , 927 – 934 ( 1993. ). - PubMed
    1. ) Yoshida , A. , Ueda , T. , Wano , Y. and Nakamura , T.DNA damage and cell killing by camptothecin and its derivative in human leukemia HL‐60 cells . Jpn. J. Cancer Res , 84 , 566 – 573 ( 1993. ). - PMC - PubMed
    1. ) Leland , H. and Weinert T. A.Checkpoints: controls that ensure the order of cell cycle events . Science , 246 , 629 – 634 ( 1989. ). - PubMed

LinkOut - more resources