Activation of the interleukin-32 pro-inflammatory pathway in response to human papillomavirus infection and over-expressionof interleukin-32 controls the expression of the humanpapillomavirus oncogene
- Authors
- Lee, Sojung; Kim, Jung-Hee; Kim, Heejong; Kang, Jeong Woo; Kim, Soo-Hyun; Yang, Young; Kim, Jinman; Park, JongSup; Park, SurNie; Hong, JinTae; Yoon, Do-Young
- Issue Date
- Mar-2011
- Publisher
- WILEY
- Keywords
- cervical cancer; cyclo-oxygenase-2; feedback inhibition; human papillomavirus E7; interleukin-32
- Citation
- IMMUNOLOGY, v.132, no.3, pp 410 - 420
- Pages
- 11
- Journal Title
- IMMUNOLOGY
- Volume
- 132
- Number
- 3
- Start Page
- 410
- End Page
- 420
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/12633
- DOI
- 10.1111/j.1365-2567.2010.03377.x
- ISSN
- 0019-2805
1365-2567
- Abstract
- P>High-risk variants of human papillomavirus (HPV) induce cervical cancer by persistent infection, and are regarded as the principal aetiological factor in this malignancy. The pro-inflammatory cytokine interleukin-32 (IL-32) is present at substantial levels in cervical cancer tissues and in HPV-positive cervical cancer cells. In this study, we identified the mechanism by which the high-risk HPV-16 E7 oncogene induces IL-32 expression in cervical cancer cells. We used antisense transfection, over-expression, or knock-down of IL-32 to assess the effects of the HPV-16 E7 oncogene on IL-32 expression in cervical cancer cells. Cyclo-oxygenase 2 (COX-2) inhibitor treatment was conducted, and the expression levels, as well as the promoter activities, of IL-32 and COX-2 were evaluated in human HPV-positive cervical cancer cell lines. E7 antisense treatment reduced the expression levels and promoter activities of COX-2, which is constitutively expressed in HPV-infected cells. Constitutively expressed IL-32 was also inhibited by E7 antisense treatment. Moreover, IL-32 expression was blocked by the application of the selective COX-2 inhibitor, NS398, whereas COX-2 over-expression resulted in increased IL-32 levels. These results show that the high-risk variant of HPV induces IL-32 expression via E7-mediated COX-2 stimulation. However, E7 and COX-2 were down-regulated in the IL-32 gamma over-expressing cells and recovered by IL-32 small interfering RNA, indicating that E7 and COX-2 were feedback-inhibited by IL-32 gamma in cervical cancer cells.
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