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Inhibition of metastasis via epithelial-mesenchymal transition in mammary tumor stem cells in response to melatonin treatment

Grant number: 13/06731-7
Support type:Scholarships in Brazil - Master
Effective date (Start): July 01, 2013
Effective date (End): June 30, 2015
Field of knowledge:Agronomical Sciences - Veterinary Medicine - Animal Pathology
Principal Investigator:Debora Aparecida Pires de Campos Zuccari
Grantee:Naiane Do Nascimento Gonçalves
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

Abstract

The breast neoplasms are the most frequent tumors in women in Brazil and the world, and also of equal importance in canine. The tumors in these two species share biological and histological characteristics, making the breast tumor in canine a model for this cancer in humans. The high mortality rate in breast cancer is mainly due to invasiveness and metastatic potential. The metastatic process, during carcinogenesis, involves a mechanism called epithelial-mesenchymal transition (EMT), characterized by a change, from an epithelial phenotype to mesenchymal identified through the loss or reduced expression of markers of epithelial cells and increased expression of mesenchymal markers. The EMT mechanism, which allows tumor cells to loosen and populate other organs, can be induced by growth factors such as transforming growth factor beta (TGF-²) which regulates cell proliferation and differentiation, migration and apoptosis. Studies have shown significant relationship between epithelial mesenchymal transition stem cells in breast cancer, which have been considered responsible for reoccurrence of the disease and resistance to chemotherapeutic treatment. That way, it becomes interesting to study potential drugs that target this specific population in breast cancer. Melatonin, a hormone secreted by the pineal gland, has tumor suppressor activity, however, little is known on its potential therapeutic effect on mammary tumor stem cells. That way, this paper intends to reproduce mamosferas from strains of human and canine breast cancer, after exposure to the growth factor TGF-², verify the inhibitory action of melatonin on the EMT mechanism. . The obtained data might confirm the anti-metastatic potential of melatonin, targeting tumor stem cells. (AU)