Antitumor activity of Metformin through p53 and cyclin D1 in the urothelial cell carcinoma

Bladder cancer is considered as one of the main drivers of cancer related mortality in adult men. Data from Global Cancer Statistics 2018 (GLOBOCAN) showed that the bladder cancer was included among the Top 10 cancer incidence in worldwide. Meanwhile, metformin, an antidiabetic agent, is believed to be able to impede the varying cancer cells expansion. Many examinations had displayed that metformin interferes via the AMPK/mTOR axis pathway, thereby suppressing tumor growth. AMPK activation can also increase stromal cell survival through p53 activation. Metformin also disrupts the cell cycle by decreasing the cyclin D1 protein in cancer cells. The human cell line 5637 was treated with metformin 15 mM, examined for cyclin D1 and p53 by immunohistochemical staining and assessed for the viability of cancer cells. The Statistic test was utilized to make a comparison of tumor viabilities and other variables. No significant differences were found in the expression of wild type p53 and cyclin D1 but significant differences were observed in the viability between the control and metformin groups. We have proven in our study that the anti-tumor effect of metformin in reducing the viability of urothelial carcinoma tumor cells not only through p53 and cyclin D1.