Heterodimerization of Bcl-2 and BcL-XL with Bax and Bad in colorectal cancer

The rate of cell loss owing to apoptosis is mediated by competitive dimerization with selective pairs of cell death antagonists (Bcl-2, BcL-X-L) and agonists (Bax, Bad). The aim of this study was to investigate which Bcl-2 family dimers had a critical factor in colorectal cancer. We analyzed the expression of Bcl-2, Bcl-X-L, Bax, and Bad in normal-appearinging mucosa and colorectal tumor tissues by Western blotting after immunoprecipitation. Compared with the ratio of Bax-Bcl-2/total Bax in normal mucosa, the ratio was significantly reduced in tumors (p = 0.02). In this series, the low ratio of Bad-Bcl-2/total Bcl-2 was associated with advanced tumor stages (p = 0.02). A reduced heterodimerization of Bax with Bcl-2 may contribute to the development of colorectal cancer. The heterodimerization of Bad with Bcl-2 may be repressed in advanced tumor tissues, and may contribute to tumor growth in colorectal cancer.