Investigation the effect of some drugs, used in the treatment of obesity, on target genes that play roles in the development of colorectal cancer

One-third of the world's population is classified as overweight or obese. With the increase in the consumption of ready-to-eat foods with urbanization, an inverse ratio emerges between the diet of the people and the amount of calories they take and the energy spent. Excessive accumulation of fat in the body and increase of negative metabolites causes various diseases. Increasing lubrication causes the formation of other types of cancer, especially colon and rectum. Cancer is a group of cells formed as a result of the uncontrolled proliferation of cells due to various reasons, the inability of the repair mechanisms involved in the cell cycle process to detect the damage, and the uncontrolled proliferation of cells not performing their functions like normal cells. The source of the dysfunction occurring in the cells occurs with the change and suppression of the expression amounts of the genes. The expression amount of tumor suppressor genes and protooncogenes that provide this order in cells changes as a result of mutation or the effect of environmental sources. As a result of these changes, the expression of tumor suppressor genes are suppressed, which prevent abnormal cells from undergoing apoptosis. As a result, cells multiply uncontrollably and abnormally. Protooncogenes take part in the cell cycle and cellular functions. In this study, in which we used colorectal cancer cell lines, we revealed how orlistat and semagulutide, which are drugs used in the treatment of obesity, affect cancer cell viability and how they affect the expression levels of some tumor suppressor and oncogenes. For this purpose, cell viability was determined by MTT assays and gene expression analyzes were determined by qRT-PCR. According to the findings, it was observed that high concentrations of orlistat decreased cell viability, while semegulitidine did not cause a significant change in cell viability. In addition, we revealed that the drugs used cause changes in the expression profiles of tumor suppressor and oncogenes in colorectal cancer cell lines.