Multiple myeloma (MM) is a B cells malignancy, described as incurable, characterized by multiple organ failure as result of bone marrow infiltration by malignant cells and systemic damage circulating monoclonal protein. Despite considerable progress in understanding the biology of MM, the molecular basis of this disease remains open to debate. The identification of new molecular markers can help to determine prognosis of cancer patients and choose the most appropriate therapy, thus contributing to improved survival rates of these patients. Previous data showed that the hypermethylation of genes DCC or TGFBR2 is significantly correlated with poor prognosis of patients affected with MM. However, as far as we investigated the involvement of proteins encoded by these genes in the tumorigenesis process of MM remains unclear. Therefore, this study aims to better understand the role of these proteins in this disease by silencing (RNAi - shRNA) or overexpression (pcDNATM3.1) of these genes in MM cell lines (RPMI-8226, SK-MM2, SKO-007 and U266) and thus elucidate the contribution of these proteins in different cellular aspects, such as, cell proliferation, adhesion, invasion, cell cycle and apoptosis. Thus, these data can provide direct evidence of the role these genes play in the biology of MM and, moreover, suggest that therapies directed at these proteins may affect the subset of patients with poor prognosis of this disease.
News published in Agência FAPESP Newsletter about the scholarship: