Elevated Expression of the cdc25A Protein Phosphatase in Colon Cancer

Elevated Expression of the cdc25A Protein Phosphatase in Colon Cancer

The nuclear protein phosphatase cdc25A has been postulated to be a protooncogene. The total nuclear phosphotyrosyl protein phosphatase (PTP) activity and the expression of cdc25A were compared in normal and cancerous colon epithelial tissue. Nuclei derived from normal mucosal epithelium and tumors w...

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Bibliographic Details
Published in:Experimental cell research Vol. 240; no. 2; pp. 236 - 243
Main Authors: Dixon, Dora, Moyana, Terence, King, Martin J.
Format: Journal Article
Language:English
Published: United States Elsevier Inc 01-05-1998
Subjects:
Animals
cdc25 Phosphatases
cdc25A
colon cancer
Colonic Neoplasms - chemically induced
Colonic Neoplasms - enzymology
Disease Models, Animal
Epithelial Cells - enzymology
mitotic index
nuclei
phosphotyrosyl protein phosphatase
Protein Tyrosine Phosphatases - metabolism
Rats
Rats, Sprague-Dawley
nuclei
cdc25A
mitotic index
phosphotyrosyl protein phosphatase
colon cancer
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Summary:The nuclear protein phosphatase cdc25A has been postulated to be a protooncogene. The total nuclear phosphotyrosyl protein phosphatase (PTP) activity and the expression of cdc25A were compared in normal and cancerous colon epithelial tissue. Nuclei derived from normal mucosal epithelium and tumors were analyzed for phosphotyrosyl protein phosphatase activity using the malachite green assay and a synthetic phosphotyrosyl peptide based on the sequence of cdc2, a known cdc25A phosphotyrosyl protein substrate. Tumorigenesis resulted in elevated nuclear PTP activity (343.0 ± 37.0% of normal epithelial PTP activity) in 52% (29 of 56) of colon tumors. In all cases elevated nuclear PTP activity correlated with an increase in the expression of cdc25A. The changes in PTP activity observed were not due to any increase in the rate of growth of the colonic mucosa as no corresponding changes occurred with PTP activity under conditions of rapid mucosal growth.
ISSN:0014-4827
1090-2422
DOI:10.1006/excr.1998.3940