Change in nicotine-induced VEGF, PGE2 AND COX-2 expression following COX inhibition in human oral squamous cancer
Autor: | Amir Amanzadeh, Mohammad Hossein Ghahremani, Mona Salimi, Bita Sedaghati, Mehrangiz Esfandiary, Sepideh Arbabi Bidgoli, Hamid Reza Aslani, Narcis Habibzadeh, Masoumeh Esfahani |
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Rok vydání: | 2013 |
Předmět: |
Vascular Endothelial Growth Factor A
Nicotine Cell Survival Health Toxicology and Mutagenesis Pharmacology Toxicology Dinoprostone Pathology and Forensic Medicine chemistry.chemical_compound Western blot Medicine Humans MTT assay Phosphorylation Extracellular Signal-Regulated MAP Kinases Carcinogen Cells Cultured Sulfonamides biology medicine.diagnostic_test Cyclooxygenase 2 Inhibitors business.industry General Medicine Vascular endothelial growth factor chemistry Celecoxib Cyclooxygenase 2 Cancer cell biology.protein Carcinoma Squamous Cell Pyrazoles Mouth Neoplasms Cyclooxygenase business medicine.drug |
Zdroj: | Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer. 31(4) |
ISSN: | 2162-6537 |
Popis: | 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. |
Databáze: | OpenAIRE |
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