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SUMMARY
Experimentation carried on inducing carcinogenesis is observed to be effective as there is a significant difference in beta actin gene expression in DMH induced carcinogenesis when compared with the control group (p<0.01). Other groups have no significant effects on increasing beta gene expression. This may be attributed to the carcinogenic effects of DMH as 1,2-dimethylhydrazine is a chemical carcinogen that causes the development of de novo tumors in the colon of rats and mice (De-Souza and Costa-Casagrande, 2018). The mechanism of action of DMH is associated primarily with DNA methylation of the stem colonocytes located at the base of the intestinal crypts, with the subsequent development of colon adenocarcinomas (Umesalma and Sudhandiran, 2010). DMH induces colonic neoplasms through cellular oxidative damage and upregulation of oncogenic pathways such as PI3K/Akt and Wnt (Yu et al., 2017). Akt, a key player in the colon tumorigenesis, inhibits the GSK3β/APC/axin-mediated degradation of β-catenin and enhances the expression of β-catenin target oncogenes, including c-Myc and cyclin D1 (Shojaei-Zarghani et al., 2020).
