Expressão gênica de MMP-2 e 9, TIMP-1 e 2, ATM, TP53, VEGF, COX-2 e CDH-1 no TVT canino

• Ano de defesa: 2014
• Autor(a) principal: Huppes, Rafael Ricardo [UNESP]
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Estadual Paulista (Unesp)
• Palavras-chave em Português: Cão - Doenças; Tumores em animais; Expressão gênica; Neovascularização; Carcinogenese; Metaloproteinase 2 da matriz; Metaloproteinase 9 da Matriz; Gene expression
• Link de acesso: http://hdl.handle.net/11449/122030

The literature reports that 1-5% of cases of primary trasmissible venereal tumor (TVT) are metastatic. Thus, it is interesting to study the mechanisms that collaborate to the metastatic invasion and implantation of TVT. Among these mechanisms, the metalloproetinases (MMP-2 and MMP-9) and their inhibitors (TIMP-1 and TIMP-2), as well as ATM, COX-2, VEGF and CDH-1 may explain the tumoral implantation in the primary site and metastatic invasion of TVT in dogs. The objectives of this study are to evaluate the gene expression of these markers and to correlate their expression with the high ability of deployment and metastatic invasion of TVT. For this study, 32 tumor samples were frozen and their mRNA were extract using the qRT-PCR method for all transcripts. The results were compared with peripheral blood of 10 healthy dogs (control group) using the Mann Whitney test. The expression of MMP-2 and TIMP-1 were significantly higher than the control group (p <0.001, p = 0.037, respectively). The expression of MMP-9 and TIMP-2 showed no statistical difference between the TVT and the control group (p = 0.535, p = 0, 906, respectively). The expression of ATM was increased in tumor tissue (TVT) when compared with the control group, while the expression of TP53 had no statistical difference between groups (p = 0.26). The evaluation of COX-2, VEGF and CDH-1 were increas in tumor tissue when compared with control group. The over expression of MMP-2 and TIMP-1 may explain the implantation ability of the tumor cells, as well as the increase of VEGF and COX-2 may explain the rapid tumor growth and the rich vasculatization. While the over expression of ATM, TP53 and CDH-1 may contribute to the low metastatic capacity of the TVT tumor