IL-8 promotes inflammatory mediators and stimulates activation of p38 MAPK/ERK-NF-kappa B pathway and reduction of JNK in HNSCC

doi:10.18632/oncotarget.16914

Chia Nan University of Pharmacy & Science Institutional Repository > 藥理學院 > 化妝品應用與管理系(所) > 期刊論文 > Item 310902800/31746

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標題:	IL-8 promotes inflammatory mediators and stimulates activation of p38 MAPK/ERK-NF-kappa B pathway and reduction of JNK in HNSCC
作者:	Chan, Leong-Perng Liu, Cheng Chiang, Feng-Yu Wang, Ling-Feng Lee, Ka-Wo Chen, Wan-Ting Kuo, Po-Lin Liang, Chia-Hua
貢獻者:	Kaohsiung Med Univ, Grad Inst Clin Med Kaohsiung Med Univ,Kaohsiung Med Univ Hosp, Dept Otolaryngol Head & Neck Surg Chi Mei Med Ctr, Div Plast Surg Chi Mei Med Ctr, HBOT Ctr Southern Taiwan Univ Sci & Technol, Dept Elect Engn Chia Nan Univ Pharm & Sci, Dept Cosmet Sci Chia Nan Univ Pharm & Sci, Inst Cosmet Sci Natl Sun Yat Sen Univ, Inst Med Sci & Technol
關鍵字:	HNSCC IL-8 inflammation MAPK
日期:	2017-08-22
上傳時間:	2018-11-30 15:55:09 (UTC+8)
出版者:	Impact Journals Llc
摘要:	This investigation identifies interleukin 8 (IL-8) as the main inflammatory mediator in head and neck squamous cell carcinoma (HNSCC). The expressions of chemokines of IL-8, IL-1 beta and IL-6 and the cytokines of tumor necrosis factor-alpha (TNF-alpha) were higher in HNSCC patient tissues than in non-cancerous matched tissues (NCMT) whereas the expression of IL-10 was lower. IL-8 is most highly expressed in the tissues of patients with HNSCC. Treatment of HNSCC cells with IL-8 increased the secretion of IL-1 beta, IL-6 and TNF-alpha and reduced IL-10 expression; the increase in the expression of IL-1 beta was particularly considerable. IL-8 silencing by siRNA reduced IL-1 beta expression in HNSCC cells, suggesting that IL-8 as a main inflammatory mediator improved IL-1 beta expression in HNSCC. The expressions of p-p38 mitogen-activated protein kinases (MAPK) and p-extracellular signal regulated kinase (p-ERK) were higher and that of p-c-Jun-NH2-terminal kinase (p-JNK) was lower in HNSCC patient tissues than in NCMT. IL-8 treatment induced p-p38 MAPK and p-ERK expression, but reduced p-JNK expressions in HNSCC cells. IL-8 siRNA suppressed p38 MAPK and ERK but increased JNK expression in HNSCC cells. Exposure of SCC25 cells to IL-8, increased the expressions of p-I kappa B-alpha and nuclear factor (NF)-kappa B, suggesting that IL-8 regulates inflammatory response by modulating the MAPK and NF-kappa B pathway in HNSCC cells. IL-8 promotes the migration of SCC25 cells and increases matrix metalloproteinase-2 (MMP-2) and MMP-9 expressions. These results reveal that IL-8 is the major stimulus of inflammatory mediation in HNSCC progression and migration by activating the p38 MAPK/ERK-NF-kappa B pathway and reducing JNK.
關聯:	Oncotarget, v.8, n.34, pp.56375-56388
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