COX-2 expression analysis and signalling pathway mechanisms in human oral squamous cell carcinoma cell lines / "Análise da expressão e mecanismos de ação da proteína COX-2 em cultura de células de carcinoma epidermóide bucal humano"

AUTOR(ES)
DATA DE PUBLICAÇÃO

2007

RESUMO

Celecoxib, a cyclooxygenase-2 (COX-2) selective nonsteroidal anti-inflammatory drug, is a new anticarcinogenic agent. Its antitumor effects depend on the one hand on its COX-2-inhibiting potency, but on the other hand on COX-2-independent mechanisms, which until now have not been fully understood. The aim of this research was to study the effects of celecoxib in growth inhibition and apoptosis induction in four Head and Neck Squamous Cell Carcinoma (HNSCC) cell lines, HN6, HN19, HN30, HN31 and HaCat an immortalized keratinocyte cell line, and verify if there is a correlation between the growth inhibition and the expression of COX-2, pAkt, ß-catenin, CD1 and NFKB. The Western Blot was used to analyze the COX-2, pAkt, ß-catenin, CD1 and NFKB protein expression level. Apoptosis induction was studied with the Annexin V kit. The cell lines proliferation will be measured through a growth curve with the Neubauer chamber and MTS method (KitCell Titer96), the proteins intracellular site was assed by immunofluorescence technic. The same cell lines without any treatment were used as controls. Results showed a significant increase in apoptotic cells index, and growth inhibition in cell lines treated with celecoxib. The proteins localization was determined through immunofluorescence. In control group the CD1 was located mostly in nucleus, after treatment CD1 nuclear localization was reduced, it could also be noticed an increase in cytoplasmic expression of ß-catenin in all cell lines while pAkt cytoplasmic increase was present exclusevely in Hn6, the other proteins maintained their cellular localization,. The Western Blot results showed considerable reduction in CD1 levels with exception of Hn19 cell line.

ASSUNTO(S)

apoptose quimioterapia cyclin d1 celecoxib cox-2 cemotherapy cox-2 apoptosis ciclina d1 celocoxib

ACESSO AO ARTIGO

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