Abstract
Colon cancer accounts for about 500,000 death cases worldwide annually and represents approximately 6.5% of cancers in Egypt. This study employed a murine colon cancer model to identify the mechanism of the therapeutic value of gallic acid or ellagic acid against colon carcinogenesis in vivo. Fifty adult male rats were distributed into five groups. Group (1) was set as a negative control group. Groups (2), (3), (4), and (5) were intrarectally injected with N-methylnitrosourea to induce colon cancer. Group (2) was kept untreated, whereas group (3) and (4) were orally administered gallic acid and ellagic acid, respectively. Group (5) received intraperitoneal injection of 5-fluorouracil. The administration of gallic acid, ellagic acid or 5-fluorouracil harmonized the hazardous effect of N-methylnitrosourea in colon cancer-afflicted rats. This was evidenced by the significant depletion in both of serum tumor associated glycoprotein-72 (TAG72) and galectin-3 (GAL3) levels as well as the significant downregulation in the expression level of frizzled-8 receptor (FRZ-8) gene and significant amplification of adenomatous polyposis coli gene expression level in the colon tissues of all treated groups. Intriguingly, such treatments resulted in a notable improvement in the pathological features of colon tissue sections of N-methylnitrosourea-challenged rats. Generally speaking, the current investigation emphasizes the favorable impact of gallic acid and ellagic acid in monitoring the progression of colon cancer in vivo. We suggest that the mitigation of Wnt signaling pathway may be the probable mechanism by which these compounds can offer their therapeutic actions against colon cancer.