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Journal of Environmental Pathology, Toxicology and Oncology
IF: 1.241 5-Year IF: 1.349 SJR: 0.519 SNIP: 0.613 CiteScore™: 1.61

ISSN Print: 0731-8898
ISSN Online: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.2013005365
pages 349-356

Change in Nicotine-Induced VEGF, PGE2 AND COX-2 Expression Following COX Inhibition in Human Oral Squamous Cancer

Mona Salimi
Departments of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran
Masoumeh Esfahani
Department of Biochemistry, Payame-Noor University, Tehran, Iran
Narcis Habibzadeh
Departments of Pharmacology and Toxicology, Faculty of Pharmacy, Islamic Azad University of Pharmaceutical Sciences, Tehran, Iran
Hamid Reza Aslani
Departments of Toxicology and Pharmacology, School of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
Amir Amanzadeh
National Cell Bank of Iran, Pasteur Institute of Iran, Tehran, Iran
Mehrangiz Esfandiary
Department of Research and Development, Pasteur Institute of Iran, Tehran, Iran
Bita Sedaghati
Department of Research and Development, Pasteur Institute of Iran, Tehran, Iran
Sepideh Arbabi Bidgoli
Departments of Pharmacology and Toxicology, Faculty of Pharmacy, Islamic Azad University of Pharmaceutical Sciences, Tehran, Iran
Mohammad Hossein Ghahremani
Departments of Toxicology and Pharmacology, School of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran; Department of Molecular Medicine, School of Advance Medical Technologies, Tehran University of Medical Sciences, Tehran, Iran

ABSTRACT

Cigarette smoke has been documented to be related to the development of cancer. However, the exact mechanism for the carcinogenic action of cigarette smoke is still unknown. Nicotine is recognized to be the major compound in cigarette smoke and has been suggested to play a role in oral cancer via a cyclooxygenase (COX)/ prostaglandin−dependent pathway. This study was designed to evaluate the action of nicotine in the oral cancer cell and to further examine whether COX-2 is responsible for expression of tumor-associated angiogenic vascular endothelial growth factor (VEGF) in vitro. Viability of human oral squamous cancer cells (BHY) was measured using MTT assay. Protein expression was determined by Western blot and immunoassay kits. We found that exposure of BHY cells to nicotine (200 µg/mL for 6 hours) resulted in 2.9-fold induction of COX-2 expression as well as a 4-fold increase in VEGF levels compared with a control group. Pretreatment with celecoxib inhibited nicotine-induced change in the expression of VEGF and COX-2. The results suggest that stimulation of COX-2 and VEGF expression can contribute as important factors in the tumorigenic action of nicotine in oral cancer progression. This effect can be blocked by celecoxib, suggesting an interaction of nicotine and COX-2 pathways.


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