Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/67705
標題: Up-Regulation of Interleukin-17 Expression by Human Papillomavirus Type 16 E6 in Nonsmall Cell Lung Cancer
作者: Chang, Y.H.
Yu, C.W.
Lai, L.C.
Tsao, C.H.
Ho, K.T.
Yang, S.C.
Lee, H.
Cheng, Y.W.
Wu, T.C.
Shiau, M.Y.
關鍵字: human papillomavirus;human papillomavirus 16 E6;Interleukin-17;Mcl-1;nonsmall cell lung cancer;epithelial-cells;proinflammatory cytokines;neutrophil recruitment;cervical tumors;in-vivo;il-17;angiogenesis;receptor;airways;growth
Project: Cancer
期刊/報告no:: Cancer, Volume 116, Issue 20, Page(s) 4800-4809.
摘要: 
BACKGROUND: Human papillomavirus (HPV) 16/18 infection is associated with nonsmoking lung cancer. In this study, the authors investigated a putative correlation between interleukin (IL)-17 expression and HPV infection in clinical nonsmall cell lung cancer (NSCLC) tissues and examined the effects of HPV infection on a human NSCLC cell line. METHODS: IL-17 expression was investigated in 79 NSCLC tumor tissues by immunohistochemistry. Growth rate, IL-17 mRNA, and secreting protein levels were also examined in HPV 16/18 E6-transfected H1299 human NSCLC cells. RESULTS: Immunohistochemical data showed that 48.1% of lung tumors had IL-17 staining, which was significantly associated with patients' sex (P=.03), HPV infection (P=.002), and tumor stage (P=.03). Significant correlations of IL-17 with IL-6 (P<.001) and IL-17 with Mcl-1 (P<.001) expression were also observed. Cell growth rate was increased, and IL-17/Mcl-1 expression levels were elevated in HPV 16 E6-transfected H1299 cells. The transfected E6 oncoproteins can significantly up-regulate expression levels of IL-17 and antiapoptotic protein Mcl-1. CONCLUSIONS: The study suggests that HPV infection-induced IL-17 levels can stimulate Mcl-1 expression through the PI3K pathway and promote lung tumor cell progression through a p53-and IL-6-independent pathway. Cancer 2010; 116: 4800-9. (C) 2010 American Cancer Society.
URI: http://hdl.handle.net/11455/67705
ISSN: 0008-543X
DOI: 10.1002/cncr.25224
Appears in Collections:期刊論文

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