Melatonin action in miRNA-155 expression in lineage of metastatic breast cancer
| Grant number: | 15/15770-1 |
| Support type: | Scholarships in Brazil - Scientific Initiation |
| Effective date (Start): | December 01, 2015 |
| Effective date (End): | November 30, 2016 |
| Field of knowledge: | Agronomical Sciences - Veterinary Medicine |
| Principal Investigator: | Debora Aparecida Pires de Campos Zuccari |
| Grantee: | Natália Mitiyo Uchiyama |
| 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 MicroRNAs are small non-coding mRNA molecules that play an important role in gene regulation. The miRNAs expression is closely associated with tumor growth, invasion, angiogenesis and metastasis of various cancer types, including breast cancer. In tumor development, angiogenesis, the formation of new blood vessels, displays a vital role, allowing tumor progression and metastasis. Thus, the search for inhibitors of this process has been a therapeutic strategy for cancer. Melatonin, a hormone produced and secreted by the pineal gland that presents oncostatic properties, is a possible treatment for breast cancer. Studies suggest that this hormone is able to modify the expression of numerous genes related to breast cancer, indicating its potential role in the regulation of miRNAs. miR-200 acts as an anti-angiogenic factor inhibiting the action of VEGF and its receptors and controlling the expression of IL-8 and CXCL1 in breast cancer. This study aims to evaluate the effect of melatonin in the modulation of miR-200 involved in the breast cancer angiogenesis in the MDA-MB-231 cell line, treated or not with melatonin and subsequent analysis of gene expression of miRNA and its target gene by real-time PCR. The results achieved may determine the possible relationship of melatonin with miR-200 and its action in the genesis of new blood vessels, and thus establish potential therapeutic protocols for control of this cellular event, crucial for a worse prognosis in patients with breast cancer. | |