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Up-regulation of interleukin-17 expression by human papillomavirus type 16 E6 in nonsmall cell lung cancer
Article first published online: 19 AUG 2010
Copyright © 2010 American Cancer Society
Volume 116, Issue 20, pages 4800–4809, 15 October 2010
How to Cite
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. and Shiau, M.-Y. (2010), Up-regulation of interleukin-17 expression by human papillomavirus type 16 E6 in nonsmall cell lung cancer. Cancer, 116: 4800–4809. doi: 10.1002/cncr.25224
- Issue published online: 24 JUN 2010
- Article first published online: 19 AUG 2010
- Manuscript Accepted: 11 DEC 2009
- Manuscript Revised: 10 DEC 2009
- Manuscript Received: 6 OCT 2009
- human papillomavirus;
- human papillomavirus 16 E6;
- nonsmall cell lung cancer
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.
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.
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.
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. © 2010 American Cancer Society.