Beta adrenergic receptor activation inhibits oral cancer migration and invasiveness

Autor(es)

Bravo-Calderon, Diego Mauricio ; Assao, Agnes ; Garcia, Natalia Galvao ; Coutinho-Camillo, Claudia Malheiros ; Roffe, Martin ; Germano, Janaina Naiara ; Oliveira, Denise Tostes

• Tipo de documento: Artigo Científico
• Fonte: ARCHIVES OF ORAL BIOLOGY; v. 118, p. 7-pg., 2020-10-01.

Resumo

Objective: The aim of this study was to verify beta 2-AR expression in oral squamous cell carcinoma cell lines (SCC-9 and SCC-25), and to investigate the role of this receptor in migration and invasion of these neoplastic cells. Design: SCC-9 and SCC-25 cells were investigated for gene and protein expression of beta 2-AR. Cell migration and invasion were analyzed by wound healing assay and transwell invasion camera system. Different concentrations (0.1, 1 and 10 mu M) of norepinephrine were used to stimulate, and 1 mu M propranolol was used to block the beta-adrenergic receptors on cancer cells. Differences in median values of SCC-9 and SCC-25 and beta 2-AR protein expression were analyzed by Friedman test and in case of significant differences; pairwise comparisons were performed using Bonferroni correction. Results: The results showed that the beta 2-AR gene and protein expression were observed in both oral cancer cell lines. The concentration of 10 mu M of norepinephrine significantly inhibited (p <= 0.05) migration of SCC-9 and SCC-25 cell lines. Furthermore, there was a significant reduction (p <= 0.05) in the effect of norepinephrine on cell migration when the beta 2-AR was inhibited by propranolol. The blockade by propranolol showed a tendency to reverse the effect of norepinephrine on the invasiveness of SCC-9 and SCC-25. Conclusions: The use of beta-adrenergic receptor agonists could become an adjuvant therapeutic target in the treatment of this malignancy. (AU)

• Processo FAPESP: 10/06333-3 - Modulação da expressão de VEGF-C por mediador relacionado ao estresse em cultura de carcinoma espinocelular de boca
• Beneficiário: Denise Tostes Oliveira
• Modalidade de apoio: Auxílio à Pesquisa - Regular