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Expression of bcl‐2, bax, and bcl‐X L proteins in azoxymethane‐induced rat colonic adenocarcinomas
Author(s) -
Hirose Yoshinobu,
Yoshimi Naoki,
Suzui Masumi,
Kawabata Kunihiro,
Tanaka Takuji,
Mori Hideki
Publication year - 1997
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/(sici)1098-2744(199705)19:1<25::aid-mc4>3.0.co;2-m
Subject(s) - azoxymethane , biology , cancer research , microbiology and biotechnology , carcinogenesis , genetics , cancer
Using western blotting and immunochemical analysis, we investigated alterations in the expression of the apoptosis‐related proteins bcl‐2, bax, and bcl‐X in colonic adenocarcinomas induced by subcutaneous injection of azoxymethane (AOM) (15 mg/kg body weight weekly for 2 wk) into male Sprague‐Dawley rats. Expression of the apoptosis‐repressor bcl‐2 in the colonic tumors was significantly weaker (0.6‐fold) than that in adjacent non‐neoplastic mucosa. The expression of bax protein, an apoptosis accelerator, was significantly stronger (7.33‐fold) in all the tumors than in the non‐tumoral mucosa. bcl‐X L protein, which functions as a repressor of apoptosis, was significantly upregulated (3.23‐fold) in all the tumors when compared with the non‐neoplastic mucosa. There was no significant difference between the expression of these proteins in the non‐neoplastic mucosa of the AOM‐treated rats and in the normal mucosa of saline‐treated control rats. As determined by immunohistochemical analysis, the tumor cells had more bax and bcl‐X protein. These findings indicate that the regulation of the apoptosis‐related proteins bcl‐2, bax, and bcl‐X L was altered in the AOM‐induced colonic neoplastic tissue. In terms of resistance to apoptosis, elevated levels bcl‐X L protein may have considerable meaning in this experimental model as well as in human colorectal cancer. Mol. Carcinog. 19:25–30, 1997. © 1997 Wiley‐Liss, Inc.