Significant coexpression of GLUT-1, Bcl-xL, and Bax in colorectal cancer.

Hypoxic cancer cells overexpress Glucose transporter 1 (GLUT-1) to accelerate glucose intake mainly for low effective, anaerobic respiration, so that they would not die of oxygen deficiency. Ischemic cell injury triggers apoptosis. Regulators of cell suicide like Bax and Bcl-xL combine their functions to cause apoptosis or to rescue cells from death. GLUT-1, Bax, and Bcl-xL are of prognostic significance in colorectal cancer but they have not been compared, yet. Thus, we aimed to determine eventual correlations between GLUT-1, Bax, and Bcl-xL in association with different clinicopathological features of colorectal cancer patients. Expressions of the proteins were evaluated in specimens of 150 colorectal patients by immunohistochemistry. The levels of tissue expressions were statistically analyzed with Spearman's correlation test. As in group of all the patients, GLUT-1 matched Bcl-xL and Bax in statistically significant manner regardless of different node status, grade of histological differentiation, histopathological type, tumor site, gender and age of patients. GLUT-1 correlated highly with Bcl-xL in both groups of various tumor growth extent: pT1 + pT2 and pT3 + pT4 tumors (P < 0.016, r = 0.6340, P < 0.0001, r = 0.5204, respectively). Bax correlated with GLUT-1 (P < 0.0001, r = 0.4284) and Bcl-xL (P < 0.0001, r = 0.5233) in pT3 and pT4 tumors without any statistical significance in a homologous comparison at pT1 and pT2 stage (P > 0.173, r = 0.1078, P > 0.744, r = 0.1, respectively). Significant coexpression of GLUT-1, Bcl-xL, and Bax could point to cooperation of these regulatory proteins in elimination due to irreversible injury, adaptation to hypoxia, reduction of further damage, and survival of colorectal cancer cells.