Abstract
Background
Physical activity is one of the modulators of the cancer risk and survival factors. Therefore, the aim of this study was considering of pre and post interval exercise training on expression of MCT-1, GLUT-1, PFK-1 and p53 as a key metabolic regulators in azoxymethane-induced experimental colon cancer
Methods
Forty-eight male BALB/c mice were equally randomized into 6 groups: I: control (C); healthy animals, II: Exercise (E), III: tumor induction (T); animals received AOM for inducing colon cancer, IV: AOM + exercise (TE); animals with colon cancer underwent 8 weeks of the interval training protocol after tumor establishment, V: exercise + AOM (ET); animals received exercise protocol one week before AOM consumption, and (VI) exercise + AOM + exercise (ETE); animals received exercise protocol one week before and after AOM consumption (about 15 weeks) Groups III-VI were weekly-received AOM (as a carcinogenic agent, 10 mg/kg s.c) in three consecutive weeks to induce colon cancer. Interval exercise training was begun at 16–18 m/min, 10–14 min, 5 days/week for 6 weeks.
Results
The results showed that the tumor significantly increased mRNA and protein of MCT1 in the tumor group compared to the control group (p < 0.001), Also, exercise before and after tumor induction reduced MCT1 (and other glucose regulators) in the colon (respectively: p < 0.02 and p < 0.01). While the p53 gene decreased significantly in the tumor group compared to the control group (p < 0.01). Exercise before tumor induction and after tumor induction increased significantly (p < 0.01 and p < 0.04 respectively) in p53 compared to the tumor group. ETE group also downregulate the expression of glucose metabolism genes in colon tumor (p < 0.05).
Conclusion
Long-term aerobic interval exercise (pre, post, pre&post tumor) can contribute to inhibition of tumor progression and treatment against colon cancer. It seems that these preventive and treatment effects exercise training can attribute to the regulation of lactate and glucose transporters by up-regulation of p53 colorectal cancer cells.