Background. The c-mos proto-oncogene was one of the first proto-oncogenes to be cloned. Apart from its role in meiosis, many efforts have been made to illuminate the mechanisms by which c-mos acts as an oncogene. c-mos or its coding messenger RNA have been confirmed in most somatic tissues at low levels. However, a detailed role of c-mos as an oncogene in somatic cells remains unknown.
Methods. In this study, we analyzed online databases to find out the correlation between Mos expression and poor survival rates in human cancer patients. Then, we investigated whether the involvement of c-mos in tumor progression via applying Apcmin intestinal cancer model and KrasG12D lung cancer model.
Results. First, we found the expression of Mos differed between human and mice, and a significant correlation between high Mos expression and poor survival rates in lung cancer patients. Interestingly, we tested that the effects of deficient c-mos in both Apcmin intestinal cancer model and KrasG12D lung cancer model. Despite the abovementioned significant correlation, the results did not show a strong inhibitory effect on murine models of lung and intestine tumors. We find no evidence of a direct role for c-mos in tumor progression in abovementioned mice models.
Discussion. It indicated that functions of c-mos gene might be species-specific and that c-mos involvement in tumor progression was circumstantial and it probably depended on other oncogene activation.
Keywords: c-mos, Kras, Apc, survival rate, murine model, lung cancer, colorectal cancer
Tet2
‐deficency in immune cells exacerbates tumor progression by increasing angiogenesis in a lung cancer model
