A direct bridge to metformin and matrix metalloproteinase relationship in prostate cancer model: oxidative stress

Abstract

Öz Purpose:The purpose of the study was to evaluate the effect of metformin as well as the possible role of Matrix metalloproteinase2 (MMP2) and oxidative stress parameters on the prostate cancer model. Materials and Methods: Male Copenhagen rats were divided into three groups. Control group, cancer group, cancer+metformin (CM) group. 2x104 Mat-LyLu cells were inoculated subcutaneously to generate prostate cancer. Metformin treatment was administered daily by gavage following inoculation of the Mat-Lylu cells. The experiment was terminated on the 14th day following Mat-LyLu cell injection. Serum glutathione (GSH), prostatespecific antigen (PSA), and malondialdehyde (MDA) levels were determined by employing the Enzyme-Linked ImmunoSorbent Assay (ELISA) method. In addition, the serum matrix metalloproteinase (MMP) 2 activities were determined via ELISA. Results: GSH was significantly increased in the CM group than in the cancer group. PSA, MDA and MMP2 were significantly lower in the CM group than in the cancer group. Oxidative stress parameters were significantly higher in the cancer group. Metformin reversed cancer's effect in GSH, PSA, MDA, and MMP2 parameters. Conclusion: Prostate cancer model caused a detrimental effect on MMP and oxidative stress parameters, and metformin administration ameliorated the changes caused by cancer. Metformin showed its mechanism of action by inhibiting free radical products originating from prostate cancer and changing the antioxidant capacity. Metformin is a candidate to be a potential anticancer drug in the therapeutic cancer treatment process.