사람 구강암종 세포주에서 Non-Steroidal Anti-Inflammatory Drug-Activated Gene(NAG-1)의 유도 및 세포고사 작용

Abstract

Background and Objectives：Nonsteroidal anti-inflammatory drug (NSAID)-activated gene (NAG-1), which is induced by NSAIDs, has proapoptotic and antitumorigenic effects in colorectal cancer cells. However, NAG-1 induction and its effect on the apoptosis in human oral cavity cancer cells (SCC 1483) have not been determined.

Materials and Method：NAG-1 expression by various NSAIDs in SCC 1483 cells was investigated by Western blot analysis. The induction of apoptosis by NSAID and the relationship between NAG-1 expression and apoptosis were determined by Western blot assay and flow cytometry. Drosophila cells stably expressing NAG-1 were constructed and NAG-1 conditioned medium (NCM) were made. Apoptosis was examined with flow cytometry on SCC 1483 cells treated with NCM.

Results：Diclofenac was the most potent inducer of NAG-1. Diclofenac inhibited the proliferation of SCC 1483 cells and this inhibition was proved as apoptosis. Diclofenac induced the expression of NAG-1 and also induced apoptosis in time and dose dependent manner. In the concentrated NCM, the expression of NAG-1 was intense and apoptosis was induced by addition of 5 μl of NCM.

Conclusion：Based on these data, we could assure that NSAIDs induced NAG-1 in oral cavity cancer cells and NAG-1 induced apoptosis. Therefore, we suggest that it is possible to use NSAIDs as a chemopreventive agent in oral cavity cancer. Further studies on the mechanism of NAG-1 and clinical use will be needed.