Areca nut components stimulate ADAM17, IL-1α, PGE2 and 8-isoprostane production in oral keratinocyte: role of reactive oxygen species, EGF and JAK signaling

被引:36
作者
Chang, Mei-Chi [1 ,2 ]
Chan, Chiu-Po [2 ]
Chen, Yi-Jane [3 ,4 ,5 ]
Hsien, Hsiang-Chi [2 ]
Chang, Ya-Ching [6 ,7 ]
Yeung, Sin-Yuet [2 ]
Jeng, Po-Yuan [8 ]
Cheng, Ru-Hsiu [3 ,4 ,5 ]
Hahn, Liang-Jiunn [3 ,4 ,5 ]
Jeng, Jiiang-Huei [3 ,4 ,5 ]
机构
[1] Chang Gung Univ Sci & Technol, Team Biomed Sci, Taoyuan, Taiwan
[2] Chang Gung Mem Hosp, Dept Dent, 199 Tung Hwa N Rd, Taipei 10591, Taiwan
[3] Natl Taiwan Univ Hosp, Sch Dent, Lab Pharmacol Toxicol & Chem Carcinogenesis, Taipei, Taiwan
[4] Natl Taiwan Univ Hosp, Dept Dent, Taipei, Taiwan
[5] Natl Taiwan Univ, Coll Med, Taipei 10764, Taiwan
[6] Mackay Mem Hospial, Dept Dent, Taipei, Taiwan
[7] Mackay Jr Coll Med Nursing & Management, Taipei, Taiwan
[8] Univ Cardenal Herrera, CEU, Sch Dent, Valencia, Spain
关键词
betel quid; oral cancer; epidermal growth factor; prostanoids; signal transduction; GROWTH-FACTOR RECEPTOR; EPITHELIAL-MESENCHYMAL TRANSITION; CELL-CYCLE ARREST; NF-KAPPA-B; OXIDATIVE-STRESS; PROSTAGLANDIN E-2; CARCINOMA-CELLS; IN-VITRO; CANCER; INFLAMMATION;
D O I
10.18632/oncotarget.7621
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Betel quid (BQ) chewing is an etiologic factor of oral submucous fibrosis (OSF) and oral cancer. There are 600 million BQ chewers worldwide. The mechanisms for the toxic and inflammatory responses of BQ are unclear. In this study, both areca nut (AN) extract (ANE) and arecoline stimulated epidermal growth factor (EGF) and interleukin-1 alpha (IL-1 alpha) production of gingival keratinocytes (GKs), whereas only ANE can stimulate a disintegrin and metalloproteinase 17 (ADAM17), prostaglandin E-2 (PGE(2)) and 8-isoprostane production. ANE-induced EGF production was inhibited by catalase. Addition of anti-EGF neutralizing antibody attenuated ANE-induced cyclooxygenase-2 (COX-2), mature ADAM9 expression and PGE(2) and 8-isoprostane production. ANE-induced IL-1 alpha production was inhibited by catalase, anti-EGF antibody, PD153035 (EGF receptor antagonist) and U0126 (MEK inhibitor) but not by alpha-naphthoflavone (cytochrome p450-1A1 inhibitor). ANE-induced ADAM17 production was inhibited by pp2 (Src inhibitor), U0126, alpha-naphthoflavone and aspirin. AG490 (JAK inhibitor) prevented ANE-stimulated ADAM17, IL-1 alpha, PGE(2) production, COX-2 expression, ADAM9 maturation, and the ANE-induced decline in keratin 5 and 14, but showed little effect on cdc2 expression and EGF production. Moreover, ANE-induced 8-isoprostane production by GKs was inhibited by catalase, anti-EGF antibody, AG490, pp2, U0126, alpha-naphthoflavone, Zinc protoporphyrin (ZnPP) and aspirin. These results indicate that AN components may involve in BQ-induced oral cancer by induction of reactive oxygen species, EGF/ EGFR, IL-1 alpha, ADAMs, JAK, Src, MEK/ERK, CYP1A1, and COX signaling pathways, and the aberration of cell cycle and differentiation. Various blockers against ROS, EGF, IL-1 alpha, ADAM, JAK, Src, MEK, CYP1A1, and COX can be used for prevention or treatment of BQ chewing-related diseases.
引用
收藏
页码:16879 / 16894
页数:16
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