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(Received for publication, July 17, 1997, and in revised form, September 19, 1997)
From the Development of colon cancer is a multistep
process frequently involving mutations in both the
APC and p53 tumor suppressor genes. In
this study we treated the HCT-116 colon cancer cell line with
alkylating agents including
N-methyl-N
Volume 272, Number 49,
Issue of December 5, 1997
pp. 30619-30622
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
COMMUNICATION:
Activation of Adenomatous Polyposis Coli (APC) Gene
Expression by the DNA-alkylating Agent
N-MethylN
-nitro-N-nitrosoguanidine
Requires p53
§
and
Sealy Center for Oncology and Hematology and
§ Department of Human Biological Chemistry and Genetics,
University of Texas Medical Branch, Galveston, Texas 77555-1048
-nitro-N-nitrosoguanidine (MNNG),which is known to cause colon cancer in animals, and
examined the expression of both APC and p53
genes. Exposure of cells with MNNG caused an 8-12-fold increase in the
level of APC mRNA and protein. APC induction was shown
to result from increased nuclear transcription of the APC
gene and correlated with a concomitant increase in the p53 protein
level after MNNG treatment. A necessary role for p53 in APC
gene regulation is supported by the failure of MNNG to induce
APC expression in cell lines either expressing very low
levels of p53 (HeLa cells) or no p53 (K562 erythroleukemia cells). The
overexpression of wild-type p53 gene into HCT-116 cells
mimicked the effect of MNNG-induced expression of APC
mRNA. A direct causal role for p53 in APC gene
regulation was further evaluated by transfecting the wild-type
p53 gene into K562 cells and observing a 5-fold increase in
the APC gene expression. These results support a model
featuring a direct link between p53 and APC in response to
alkylation-induced DNA damage and suggest a novel role for p53 in a
stress-response pathway involving APC.
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