Relationship with Metalloproteinase 13, E-cadherin, Homocysteine and Co Factors Folic Acid and Vitamin B12 in Patients Diagnosed with Prostate Cancer

Abstract

Introduction:: Prostate cancer (Pc) is the most frequent neoplasia in men and the second cause of death in Brazil. Objective:: To analyze the interactions and biologicals responses of Pc oxidative stress and prostatespecific antigen (PSA), E-cadherin and MMP-13. Demonstrate whether the increase of the amount of the form of E-cadherin found in the plasma of Pc patients, correlates with decrease of the PSA. Methods:: Samples were obtained through peripheral venipuncture to analyse parameters of biomarkers pc as PSA, E-cadherin, MMP-13, Homocysteine, Folic acid, Vitamin B12, Testosterone T and free following the patients diagnosis, 3 and 6 months during their treatment to analyze the biological responses of Pc oxidative stress. Results:: The analysis was performed by using immunoenzymatic assay. Statistical data processed through Excel in Windows Vista and analyzed through the Shapiro-wilk Test, ANOVA, and Spearman Test. An increase in the concentration of E-cadherin (p = 0.02), as a decrease in concentration of PSA (p < 0.001), total testosterone (p < 0.001) and free testosterone (p = 0.02) was observed during the treatment period without significant alterations in the remaining markers for either of the periods. Discussion:: It was found that during treatment of men diagnosed with pc that there was an an increase in the concentration of plasmatic E-cadherin, which was negatively correlated with the concentrations of folic acid (-0,03 (0,87) rs (p). It was observed that the levels of hcy are positively correlated with concentrations of total testosterone and a negative correlation. Vitamins B12 remained within the parameters of normality during the entire study. Conclusion:: P.S.A levels were free and total testosterone levels decreased. In this way, monitoring the folic acid, E-cadherin dosages of patients during the treatment phases can effectively complement in the face of remission, since it would be a way of preventing abnormal cell replications, with a clinical view prudent so that the cell methylation cycle is not affected.