MICRO-RNAS EXPRESSION IN NORMAL AND TUMORAL PROSTATIC EPITHELIAL CELLS TREATED WITH FINASTERIDE.

• Grant number: 10/05042-5
• Support Opportunities: Scholarships in Brazil - Post-Doctoral
• Start date: August 01, 2010
• End date: January 31, 2013
• Field of knowledge: Biological Sciences - Morphology - Cytology and Cell Biology
• Principal Investigator: Sérgio Luis Felisbino
• Grantee: Flávia Karina Delella
• Host Institution: Instituto de Biociências (IBB). Universidade Estadual Paulista (UNESP). Campus de Botucatu. Botucatu , SP, Brazil

Abstract

Prostate cancer (PCa) is the most commonly diagnosed and the second cause of cancer death among men in America and Western Europe. In Brazil, the number of PCa new cases valuated for 2010 will be 52.350. PCa development and progression are slow processes and includes genetic and epigenetic alterations that promote an imbalance between molecular ways that control proliferation, differentiation and apoptosis. This significant period of latency is considered an important time to adopt chemoprevention against PCa. Recently, the finasteride, a type 2 5±-reductase inhibitor used in the benign prostatic hyperplasia treatment, was approved to be used in the PCa chemoprevention by the American Society of Urology. However, some medical academic communities think that more studies are necessary to approve a safety use of the finasteride in PCa chemoprevention. Recent studies have been shown that human tumors present epigenetic alterations, like altered micro-RNA expression. These small RNAs have been considered new oncogenes or tumor suppressors, which can be used as a major tool for cancer diagnosis, staging and prognosis. Currently, there are few studies relating the expression profile or the functional role of micro-RNAs in PCa. Thereby, considering the importance of PCa prevention and the doubts about finasteride effects, the aim of this project is investigate finasteride effects over oncogenes and tumor suppressions micro-RNAs expression in normal and tumoral prostatic cells.