Induction of Non-Steroidal Anti-Inflammatory Drug-Activated Gene(NAG-1) in Human Oral Cavity Cancer Cells and its Effect on Apoptosis.
- Author:
Joo Hwan LEE
1
;
Joo Heon YOON
;
Jeung Gweon LEE
;
Jung Hyun CHANG
;
Yoon Jae LEE
;
Kyung Su KIM
Author Information
1. Department of Otorhinolaryngology, Yong Dong Severance Hospital, Yonsei University College of Medicine, Seoul, Korea. ydrhinol@yumc.yonsei.ac.kr
- Publication Type:Original Article
- Keywords:
Non-steroidal anti-inflammatory agents;
Oral cancers;
Apoptosis
- MeSH:
Anti-Inflammatory Agents, Non-Steroidal;
Apoptosis*;
Blotting, Western;
Colorectal Neoplasms;
Culture Media, Conditioned;
Diclofenac;
Drosophila;
Flow Cytometry;
Humans*;
Mouth Neoplasms;
Mouth*
- From:Korean Journal of Otolaryngology - Head and Neck Surgery
2004;47(10):1030-1037
- CountryRepublic of Korea
- Language:Korean
-
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 mu 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.
