S-Space College of Medicine/School of Medicine (의과대학/대학원) Otorhinolaryngology (이비인후과학전공) Journal Papers (저널논문_이비인후과학전공)
Celecoxib inhibits cell proliferation through the activation of ERK and p38 MAPK in head and neck squamous cell carcinoma cell lines
- Park, Seok-Woo; Kim, Hyo-Sun; Hah, Jeong-Whun; Jeong, Woo-Jin; Sung, Myung-Whun; Kim, Kwang-Hyun
- Issue Date
- LIPPINCOTT WILLIAMS & WILKINS
- ANTI-CANCER DRUGS; Vol.21 9; 823-830
- It has been observed that several cyclooxygenase-2 (COX-2) inhibitory chemicals might inhibit proliferation of various cancer cells through COX-2-independent action. We also identified that celecoxib more selectively kills cell lines derived from head and neck squamous cell carcinoma (HNSCC) than its non-cancerous counterparts, irrespective of COX-2 expression. Herein, we investigated whether the regulation of mitogen-activated protein kinases activity might be one of the main mechanisms related to a conspicuous COX-2-independent tumor-killing effect of celecoxib in HNSCC cell lines. We assessed the effect of celecoxib on extracellular signal-regulated kinase (ERK), p38, and c-Jun NH2-terminal kinase activity by a transcription factor activation assay then evaluated, if these factors might be involved in the COX-2-independent tumor-killing effect of celecoxib by blocking their activity. We found that the blocking activation of ERK and/or p38 could reverse the celecoxib-induced cell growth inhibition by 50-80% in HNSCC cell lines, but it was not tested in cancer cells of other types. In conclusion, our study suggests that most COX-2-independent tumor-killing action of celecoxib is mediated by the upregulation of ERK and/or p38 activity in HNSCC cells. These results encourage investigation on the underlying mechanisms and detailed outcomes of mitogen-activated protein kinases activation by celecoxib more concisely, for using its excellent tumor-killing effect more safely in the clinical field of cancer treatment. Anti-Cancer Drugs 21:823-830 (C) 2010 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
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