Differential induction of heme oxygenase-1 against nicotine-induced cytotoxicity via the PI3K, MAPK, and NF-kappa B pathways in immortalized and malignant human oral keratinocytes

Journal of Oral Pathology & Medicine : Official Publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
Hwa-Jeong LeeEun-Cheol Kim

Abstract

Heme oxygenase-1 (HO-1) exhibits cytoprotective effects in many different cell types and is induced by nicotine exposure in human gingival fibroblasts. However, the role of HO-1 in cancer cells exposed to nicotine has not previously been described. We investigated the effects of nicotine on HO-1 protein expression and cell viability in immortalized (IHOK) and malignant (HN12) human oral keratinocyte cells using the 3,4,5-dimethylthiazol-2-yl-2,5-diphenyl tetrazolium bromide assay and Western blotting. We also examined the involvement of the phosphoinositide-3-kinase (PI3K), mitogen-activated protein kinase (MAPK), and nuclear factor-kappaB (NF-kappaB) signaling pathways in nicotine-induced cytotoxicity and HO-1 levels in IHOK and HN12 cells. Nicotine-induced HO-1 production and had cytotoxic effects on cells in both a concentration- and time-dependent manner. Nicotine-induced cytotoxicity and accumulation of HO-1 were greater in IHOK cells than in HN12 cells. Molecular inhibitors of the ERK, p38 MAP kinase, PI3 K, and NF-kappaB signaling pathways blocked the cytotoxic effects and induction of HO-1 expression by nicotine. Treatment with antioxidants (bilirubin, N-acetylcysteine) protected cells against nicotine-induced cytotoxic...Continue Reading

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Citations

Jul 6, 2010·International Immunopharmacology·Catherine LombardRobert J McKallip
Jun 19, 2009·The Journal of Investigative Dermatology·Ikuko NumataSetsuya Aiba
Oct 2, 2012·Archives of Oral Biology·Hiroyo KarubeMasato Matsuoka
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Sep 24, 2010·Oral Diseases·W FanH He

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