Fibronectin expression is decreased in metastatic renal cell carcinoma following endostatin gene therapy

Autor(es)

Barbosa Chaves, Karen Cristina ^[1] ; Turaca, Lauro Thiago ^[2] ; Pesquero, Joao Bosco ^[2] ; Mennecier, Gregory ^[3] ; Zaidan Dagli, Maria Lucia ^[3] ; Chammas, Roger ^[4] ; Schor, Nestor ^[1] ; Bellini, Maria Helena ^{[1, 5]}

Afiliação do(s) autor(es)

^[1] Univ Fed Sao Paulo, Dept Med, Div Nephrol, Sao Paulo - Brazil

^[2] Univ Fed Sao Paulo, Dept Biophys, Sao Paulo - Brazil

^[3] Univ Sao Paulo, Sch Vet Med & Anim Sci, Dept Pathol, Sao Paulo - Brazil

^[4] Univ Sao Paulo, Dept Radiol, Sao Paulo - Brazil

^[5] Univ Sao Paulo, IPEN CNEN, Dept Biotechnol, Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: BIOMEDICINE & PHARMACOTHERAPY; v. 66, n. 6, p. 464-468, SEP 2012.
• Citações Web of Science: 9

Resumo

Tumor cells induce the disruption of homeostasis between cellular and extracellular compartments to favor tumor progression. The expression of fibronectin (FN), a matrix glycoprotein, is increased in several carcinoma cell types, including renal cell carcinoma (RCC). RCC are highly vascularized tumors and are often amenable to antiangiogenic therapy. Endostatin (ES) is a fragment of collagen XVIII that possesses antiangiogenic activity. In this study, we examined the modulation of FN gene expression by ES gene therapy in a murine metastatic renal cell carcinoma (mRCC) model. Balb/C mice bearing Renca cells were treated with NIH/3T3-LXSN cells or NIH/3T3-LendSN cells. At the end of the experiment, the ES serum levels were measured, and the FN gene expression was assessed using real-time PCR. The tissue FN was evaluated by western blotting and by immunofluorescence analysis. The ES serum levels in treated mice were higher than those in the control group (P < 0.05). ES treatment led to significant decreases at the FN mRNA (P < 0.001) and protein levels (P < 0.01). Here, we demonstrate the ES antitumor effect that is mediated by down-regulation of FN expression in mRCC. (C) 2012 Elsevier Masson SAS. All rights reserved. (AU)

• Processo FAPESP: 09/12518-9 - Avaliação da expressão de moléculas de adesão (VCAM e ICAM) no carcinoma renal metastático pulmonar de animais submetidos à terapia gênica com a endostatina
• Beneficiário: Karen Cristina Barbosa Chaves
• Modalidade de apoio: Bolsas no Brasil - Mestrado
• Processo FAPESP: 10/18969-0 - Estudo da regulação do NF-kB no carcinoma renal metastático após terapia gênica com endostatina
• Beneficiário: Maria Helena Bellini Marumo
• Modalidade de apoio: Auxílio à Pesquisa - Regular