Soluble interleukin-6 receptor activates the human papillomavirus type 18 long control region in SW756 cervical carcinoma cells in a STAT3-dependent manner

被引：18

作者：

Smola-Hess, S ^{[1
]}

de Silva, US ^{[1
]}

Hadaschik, D ^{[1
]}

Pfister, HJ ^{[1
]}

机构：

[1] Univ Cologne, Inst Virol, D-50935 Cologne, Germany

来源：

JOURNAL OF GENERAL VIROLOGY | 2001年 / 82卷

关键词：

D O I：

10.1099/0022-1317-82-10-2335

中图分类号：

Q81 [生物工程学（生物技术）]; Q93 [微生物学];

学科分类号：

071005 ; 0836 ; 090102 ; 100705 ;

摘要：

Cervical carcinoma cells producing high levels of interleukin-6 (IL-6) were shown to be unresponsive to the cytokine IL-6 due to the loss of their IL-6 receptor. Addition of IL-6 receptor in a soluble form restores IL-6 signalling in SW756 carcinoma cells. This leads to a rapid and strong activation of the transcription factor signal transducer and activator of transcription 3 (STAT3). Nuclear factor IL-6 (NF-IL6, C/EBP beta) was induced only as a late event. While C/EBP beta significantly repressed the human papillomavirus type 18 long control region (HPV18-LCR), IL-6 signalling unexpectedly activated the HPV18-LCR in these cells. This IL-6 receptor-mediated induction could be completely reverted by transfection of a dominant-negative STAT3 but not STAT1 expression construct, indicating that STAT3 might play an important role in HPV18 oncogene promoter activation.

引用

页码：2335 / 2339

页数：5

共 34 条

[11] Loss of IL-6 receptor expression in cervical carcinoma cells inhibits autocrine IL-6 stimulation: Abrogation of constitutive monocyte chemoattractant protein-1 production [J].