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Action of melatonin on the induction of apoptosis by interleukin 25 in breast tumor lines

Grant number: 12/11965-4
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): October 01, 2012
Effective date (End): September 30, 2013
Field of knowledge:Health Sciences - Medicine
Principal Investigator:Debora Aparecida Pires de Campos Zuccari
Grantee:Mariana Castilho Facchini
Home Institution: Faculdade de Medicina de São José do Rio Preto (FAMERP). Secretaria de Desenvolvimento Econômico (São Paulo - Estado). São José do Rio Preto , SP, Brazil


Cytokines are intercellular mediators which regulate survival, differentiation and effector functions of cells and has been proven to be related to cancer. Some of them have definite activity, but the understanding of its interaction with the genesis and tumor progression may contribute to the success of preventive and therapeutic protocols. The IL-25, also called IL-17E, is known for her role in the immune response by promoting inflammation and stimulate the production of inflammatory cytokines. It is known that the interaction with its receptor IL-25R, when present, induce apoptosis and this is called anti-cytokine tumor. However, little is known about this interaction, only that there is competition for the site of action with IL-17B in neoplastic cells, contributing to tumor progression. It has been proposed that melatonin may protect normal cells from apoptosis, and conversely, induce it in neoplastic cells. The objective of this study is to control tumor growth through increased apoptosis as a therapeutic strategy in breast cancer and this will be accomplished treatment with IL-25 with or without melatonin in breast cancer lines MCF 7, MDA-MB-231 and normal epithelial cell line (MCF-10A). These results could allow the use of interleukins associated or not with melatonin as therapeutic agents in breast cancer.