Wild-type p53 restores cell cycle control and inhibits gene amplification in cells with mutant p53 alleles.

Abstract:

:Loss of cell cycle control and acquisition of chromosomal rearrangements such as gene amplification often occur during tumor progression, suggesting that they may be correlated. We show here that the wild-type p53 allele is lost when fibroblasts from patients with the Li-Fraumeni syndrome (LFS) are passaged in vitro. Normal and LFS cells containing wild-type p53 arrested in G1 when challenged with the uridine biosynthesis inhibitor PALA and did not undergo PALA-selected gene amplification. The converse occurred in cells lacking wild-type p53 expression. Expression of wild-type p53 in transformants of immortal and tumor cells containing mutant p53 alleles restored G1 control and reduced the frequency of gene amplification to undetectable levels. These studies reveal that p53 contributes to a metabolically regulated G1 check-point, and they provide a model for understanding how abnormal cell cycle progression leads to the genetic rearrangements involved in tumor progression.

journal_name

Cell

journal_title

Cell

authors

Yin Y,Tainsky MA,Bischoff FZ,Strong LC,Wahl GM

doi

10.1016/0092-8674(92)90244-7

subject

Has Abstract

pub_date

1992-09-18 00:00:00

pages

937-48

issue

6

eissn

0092-8674

issn

1097-4172

pii

0092-8674(92)90244-7

journal_volume

70

pub_type

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