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Transcriptional regulation of human papillomavirus type 16 LCR by different C/EBPβ isoforms
Author(s) -
Struyk Linda,
Meijden Els van der,
Minnaar René,
Fontaine Véronique,
Meijer Ingeborg,
Schegget Jan ter
Publication year - 2000
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/(sici)1098-2744(200005)28:1<42::aid-mc6>3.0.co;2-8
Subject(s) - biology , gene isoform , human papillomavirus , microbiology and biotechnology , genetics , gene , medicine
During genital human papillomavirus (HPV) infection several cytokines are released, such as interleukin‐1 (IL‐1), tumor necrosis factorα (TNFα), IL‐6, and IL‐8. These cytokines may play a role in the immune surveillance against viral infection. Two of these cytokines, IL‐1 and TNFα, suppress the transcription of the HPV16 early genes. CAATT/enhancer binding proteinβ (C/EBPβ), which is activated by IL‐1 and TNFα, has been suggested to act as a mediator of this transcriptional downregulation. C/EBPβ contains three different translation initiation sites that can lead probably by leaky ribosome scanning to the generation of three isoforms of C/EBPβ, namely full‐length C/EBPβ, liver enriched transcriptional activator protein (LAP), and liver enriched inhibitory protein (LIP). When transiently expressed in C33A and HeLa cells, the first two C/EBPβ isoforms activate the HPV16 long control region (LCR). LIP, which acts as an antagonist of C/EBPβ, represses the HPV16 LCR activity. Our observation that treatment of HeLa cells with IL‐1 leads to induction of LIP supports the hypothesis that the LCR downregulation by IL‐1 is mediated by LIP. Mol. Carcinog. 28:42–50, 2000. © 2000 Wiley‐Liss, Inc.