Expression of bcl-2, bax, and bcl-XL proteins in azoxymethane-induced rat colonic adenocarcinomas

✍ Scribed by Yoshinobu Hirose; Naoki Yoshimi; Masumi Suzui; Kunihiro Kawabata; Takuji Tanaka; Hideki Mori

• Publisher: John Wiley and Sons
• Year: 1997
• Tongue: English
• Weight: 281 KB
• Volume: 19
• Category: Article
• ISSN: 0899-1987
• DOI: 10.1002/(sici)1098-2744(199705)19:1<25::aid-mc4>3.0.co;2-m

✦ Synopsis

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.