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Mol. Cells 2010; 29(2): 185-194

Published online February 28, 2010

https://doi.org/10.1007/s10059-010-0026-y

© The Korean Society for Molecular and Cellular Biology

Anti-Cancer Effects of Celecoxib in Head and Neck Carcinoma

Young-Youn Kim, Eun-Jin Lee, Yu-Kyoung Kim1, Soung-Min Kim, Ju-Yong Park2, Hoon Myoung*, and Myung-Jin Kim

Department of Oral and Maxillofacial Surgery, School of Dentistry, Seoul National University, Seoul 110-749, Korea, 1Dental Research Institute, Seoul National University, Seoul 110-749, Korea, 2Department of Oral Oncology, National Cancer Center, Goyang 410-769, Korea

Correspondence to : *Correspondence: myoungh@snu.ac.kr

Received: September 25, 2009; Revised: November 11, 2009; Accepted: November 12, 2009

Abstract

Although many studies highlighted cyclooxygenase2 (COX2) inhibition as a promising therapeutic strategy for cancer, more evidence is needed for clinical application. The purpose of this study was to investigate the fea-sibility of COX2 inhibition as a strategic treatment modality for head and neck carcinoma (HNC). We tested COX2 inhibitor, celecoxib in six types of HNC cells and analyzed the expression changes in proteins related to angiogenesis and apoptosis in vitro. We also evaluated proliferation, gelatinolysis and in vitro invasion. We used a hamster carcinogenesis model and a mouse tumorigenesis model for the in vivo evaluation of COX2 inhibition. We performed immunohistochemistry to assess changes in the expression of COX2, survivin and angiogenesis. Celecoxib administration caused decreases in the expressions of COX2, VEGF and survivin in vitro. Proliferation, in vitro invasion and gelatinolytic activity were reduced in HNC cell lines, but the effect was inconsistent across lines. COX2 inhibition retarded oral carcinogenesis from an early carcinogenic stage with increased apoptosis and decreased survivin expression. COX2 inhibition did not inhibit tumor growth, even with the COX2 downregulation and decrease in neovascularization. We conclude that COX2 inhibition has a chemopreventive effect, but its application as a treatment of HNC in a clinical setting still requires further research to overcome its limited anti-cancer effects.

Keywords , celecoxib, cyclooxygenase2 (COX2), head and neck carcinoma (HNC), invasion, oral squamous cell carcinoma

Article

Research Article

Mol. Cells 2010; 29(2): 185-194

Published online February 28, 2010 https://doi.org/10.1007/s10059-010-0026-y

Copyright © The Korean Society for Molecular and Cellular Biology.

Anti-Cancer Effects of Celecoxib in Head and Neck Carcinoma

Young-Youn Kim, Eun-Jin Lee, Yu-Kyoung Kim1, Soung-Min Kim, Ju-Yong Park2, Hoon Myoung*, and Myung-Jin Kim

Department of Oral and Maxillofacial Surgery, School of Dentistry, Seoul National University, Seoul 110-749, Korea, 1Dental Research Institute, Seoul National University, Seoul 110-749, Korea, 2Department of Oral Oncology, National Cancer Center, Goyang 410-769, Korea

Correspondence to:*Correspondence: myoungh@snu.ac.kr

Received: September 25, 2009; Revised: November 11, 2009; Accepted: November 12, 2009

Abstract

Although many studies highlighted cyclooxygenase2 (COX2) inhibition as a promising therapeutic strategy for cancer, more evidence is needed for clinical application. The purpose of this study was to investigate the fea-sibility of COX2 inhibition as a strategic treatment modality for head and neck carcinoma (HNC). We tested COX2 inhibitor, celecoxib in six types of HNC cells and analyzed the expression changes in proteins related to angiogenesis and apoptosis in vitro. We also evaluated proliferation, gelatinolysis and in vitro invasion. We used a hamster carcinogenesis model and a mouse tumorigenesis model for the in vivo evaluation of COX2 inhibition. We performed immunohistochemistry to assess changes in the expression of COX2, survivin and angiogenesis. Celecoxib administration caused decreases in the expressions of COX2, VEGF and survivin in vitro. Proliferation, in vitro invasion and gelatinolytic activity were reduced in HNC cell lines, but the effect was inconsistent across lines. COX2 inhibition retarded oral carcinogenesis from an early carcinogenic stage with increased apoptosis and decreased survivin expression. COX2 inhibition did not inhibit tumor growth, even with the COX2 downregulation and decrease in neovascularization. We conclude that COX2 inhibition has a chemopreventive effect, but its application as a treatment of HNC in a clinical setting still requires further research to overcome its limited anti-cancer effects.

Keywords: , celecoxib, cyclooxygenase2 (COX2), head and neck carcinoma (HNC), invasion, oral squamous cell carcinoma

Mol. Cells
Aug 31, 2022 Vol.45 No.8, pp. 513~602
COVER PICTURE
Cryo-EM structure of human porphyrin transporter ABCB6 (main figure) shows that binding of hemin (inset, magenta) in concert with two glutathione molecules (cyan) primes ABCB6 for high ATP turnover (Kim et al., pp. 575-587).

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