Reduced UV-induced mutations in human osteosarcoma cells stably expressing transfected wild-type p53 cDNA

被引:10
作者
Yagi, T
Mohri-Nakanishi, K
Natsuda, T
Yamagishi, N
Miyakoshi, J
Takebe, H
机构
[1] Kyoto Univ, Grad Sch Med, Dept Radiat Genet, Sakyo Ku, Kyoto 60601, Japan
[2] Kyoto Univ, Res Ctr Environm Qual Control, Otsu, Shiga 520, Japan
关键词
UV-induced mutations; human osteosarcoma cells; wild-type p53 cDNA;
D O I
10.1016/S0304-3835(97)00406-0
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
We constructed the plasmid which can express human wild-type p53 cDNA and introduced it into the human osteosarcoma cell line SAOS-2 that lacks the chromosomal p53 gene. A cell clone stably expressing p53 protein was isolated and UV sensitivity and UV-induced mutation frequencies of the clone were examined. The UV sensitivity of the clone was slightly higher and UV-induced hprt mutation frequencies of the clone were markedly lower than those of parental SAOS-2 cells. The capability to repair UV-induced DNA damage assessed by the amount of unscheduled DNA synthesis or DNA single strand breaks as well as cell cycle progression after UV irradiation were not different between the clone and SAOS-2 cells. These results indicate that wild-type p53 protein would be involved in the human DNA damage-processing pathway other than the genome-overall excision repair. (C) 1998 Elsevier Science Ireland Ltd.
引用
收藏
页码:71 / 76
页数:6
相关论文
共 21 条
[1]  
BIRNBOIM HC, 1981, CANCER RES, V41, P1892
[2]   THE ROLE OF P53 IN REGULATING GENOMIC STABILITY WHEN DNA AND RNA-SYNTHESIS ARE INHIBITED [J].
CHERNOVA, OB ;
CHERNOV, MV ;
AGARWAL, ML ;
TAYLOR, WR ;
STARK, GR .
TRENDS IN BIOCHEMICAL SCIENCES, 1995, 20 (10) :431-434
[3]   CELLULAR-RESPONSES TO DNA-DAMAGE - CELL-CYCLE CHECKPOINTS, APOPTOSIS AND THE ROLES OF P53 AND ATM [J].
ENOCH, T ;
NORBURY, C .
TRENDS IN BIOCHEMICAL SCIENCES, 1995, 20 (10) :426-430
[4]   LI-FRAUMENI SYNDROME FIBROBLASTS HOMOZYGOUS FOR P53 MUTATIONS ARE DEFICIENT IN GLOBAL DNA-REPAIR BUT EXHIBIT NORMAL TRANSCRIPTION-COUPLED REPAIR AND ENHANCED UV RESISTANCE [J].
FORD, JM ;
HANAWALT, PC .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (19) :8876-8880
[5]   INCREASED UV-INDUCED SCES BUT NORMAL REPAIR OF DNA-DAMAGE IN P53-DEFICIENT MOUSE CELLS [J].
ISHIZAKI, K ;
EJIMA, Y ;
MATSUNAGA, T ;
HARA, R ;
SAKAMOTO, A ;
IKENAGA, M ;
IKAWA, Y ;
AIZAWA, S .
INTERNATIONAL JOURNAL OF CANCER, 1994, 58 (02) :254-257
[6]   TRANSFECTED MUTANT P53 GENE INCREASES X-RAY-INDUCED CELL-KILLING AND MUTATION IN HUMAN FIBROBLASTS IMMORTALIZED WITH 4-NITROQUINOLINE 1-OXIDE BUT DOES NOT INDUCE NEOPLASTIC TRANSFORMATION OF THE CELLS [J].
KAWASHIMA, K ;
MIHARA, K ;
USUKI, H ;
SHIMIZU, N ;
NAMBA, M .
INTERNATIONAL JOURNAL OF CANCER, 1995, 61 (01) :76-79
[7]   CANCER - P53, GUARDIAN OF THE GENOME [J].
LANE, DP .
NATURE, 1992, 358 (6381) :15-16
[8]   P53 AND ITS 14 KDA C-TERMINAL DOMAIN RECOGNIZE PRIMARY DNA-DAMAGE IN THE FORM OF INSERTION DELETION MISMATCHES [J].
LEE, S ;
ELENBAAS, B ;
LEVINE, A ;
GRIFFITH, J .
CELL, 1995, 81 (07) :1013-1020
[9]   REARRANGEMENT OF THE P53 GENE IN HUMAN OSTEOGENIC SARCOMAS [J].
MASUDA, H ;
MILLER, C ;
KOEFFLER, HP ;
BATTIFORA, H ;
CLINE, MJ .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1987, 84 (21) :7716-7719
[10]   PRIMARY STRUCTURE POLYMORPHISM AT AMINO-ACID RESIDUE-72 OF HUMAN-P53 [J].
MATLASHEWSKI, GJ ;
TUCK, S ;
PIM, D ;
LAMB, P ;
SCHNEIDER, J ;
CRAWFORD, LV .
MOLECULAR AND CELLULAR BIOLOGY, 1987, 7 (02) :961-963