TGF-beta1 and IL-4 downregulate human papillomavirus-16 oncogene expression but have differential effects on the malignant phenotype of cervical carcinoma cells

Virus Research
Manuela DonalisioDavid Lembo

Abstract

Host immune response to human papillomavirus (HPV) is a crucial factor in viral clearance and control of persistent infections. The existence of an intercellular control mechanism mediated by cytokines to suppress HPV-gene transcription and to prevent malignant conversion of HPV-infected cells, has been postulated. In a previous study, we demonstrated the inhibitory activity of several cytokines on the HPV-16 long control region (LCR)-driven transcription; among these, IL-4 was reported as a LCR inhibitor for the first time and proposed as a candidate for further studies. Here, we addressed the question of whether IL-4 represses HPV-16 oncogene transcription and exerts antitumor activity in HPV-16 positive cervical carcinoma cell lines. Results indicated that downregulation of E6 and E7 levels by IL-4 in CaSki cells is weaker than that exerted by TGF-beta1, a known LCR inhibitor, although both cytokines are equally active in suppressing LCR-driven transcriptional activity in a reporter cell line. Moreover, only TGF-beta rescued p53 expression, Rb response pathway, and induced cellular senescence. SiHa cells were unresponsive to both cytokines. These findings suggest that the two cytokines may play a role in the control of HPV i...Continue Reading

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Citations

Jun 7, 2014·Journal of Medicinal Chemistry·Manuela DonalisioOriana Tabarrini
Sep 2, 2016·Archives of Virology·Manik GhoshManuela Donalisio
Jan 5, 2011·Immunological Reviews·Purnima BhatGraham R Leggatt
Mar 25, 2016·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Haiyan ZhuXueqiong Zhu
Apr 25, 2013·Clinical and Experimental Dermatology·H J ParkH Y Choi

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