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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 KCI 등재

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대한구강악안면병리학회지 (The Korean Journal of Oral and Maxillofacial Pathology)
대한구강악안면병리학회 (Korean Academy Of Oral And Maxillofacial Pathology)
초록

Heme oxygenase-l (HO-l) exhibits cyt oprotective effects in many different cell types and is induced by nicotine exposure in human gingival fibroblasts‘ However‘ therole of HO- l in cancer cells exposed to nicotine has not previously been descnbed We investigated the effects of nicotine on HO-l protein expression and cell viability in immortalized (IHOK) and malignant (HN12) human ora l keratinocyte cells using the MTT assay and Western blotting. We al so examined the involvement of t he phosphoinosit ide-3-0H- kinase (PI3K), mitogen-acti vated protein kinase (MAPK) , and nucJear factor-κ B (NF-κ B) signaling pathways in nicotine-induced cytotoxicity and HO- l levels in IHOK and HN12 cell s‘ Nicotine induced HO- l pro ducti on and had cytotoxic effects on cells in both a concentration- and time-dependent manner. Nicotine-induced cytotox icity and accumulation of HO- l were greater in JJ-IOK cells than in HN12 cells Molecular inhibitors of the ERK, p38 MAP kinase, PI3K, and NF-κ B signaling pathways blocked the cytotoxic effects and induction of J-IO-l expression by nicotine. Treatmen t with an t ioxida nts (bil irubin, N-acetyl cysteine) protected cells against nicotine-induced cytotoxicity and blocked the upregula tion of J-IO- l, the effects of which were more pronounced in II-IOK cells than in HN12 cells Collecti vely, these results suggest that J-IO- l plays a principal role in the protective response to nicotine in oral cancel and immortalized keratinocytes. Moreover, the addition of exogenous antioxidants may help to protect oral epithelial cells as chemopreventive agents against nicotine-induced oxidative stress.

저자
  • Hwa-Jeong Lee(Department of Oral & Maxillofacial Pathology, College of Dentistry, Wonkwang University)
  • Jun Lee(Department of Oral & Maxillofacial Pathology, College of Dentistry, Wonkwang University)
  • Seung-Ki Min(Department of Oral & Maxillofacial Pathology, College of Dentistry, Wonkwang University)
  • Han-Young Guo(Department of Oral & Maxillofacial Pathology, College of Dentistry, Wonkwang University)
  • Sun-Kyung Lee(Department of Oral & Maxillofacial Pathology, College of Dentistry, Wonkwang University)
  • Suk-Keun Lee(Department of Oral & Maxillofacial Pathology, College of Dentistry, Wonkwang University)
  • Eun-Cheol Kim(Department of Oral & Maxillofacial Pathology, College of Dentistry, Wonkwang University)