ArticleJournal of virology1991
Epidermal growth factor (EGF) elicits down-regulation of human papillomavirus type 16 (HPV-16) E6/E7 mRNA at the transcriptional level in an EGF-stimulated human keratinocyte cell line: functional role of EGF-responsive silencer in the HPV-16 long control region.
Article in Journal of virology, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 35 citations in OpenAlex.
- MEK/ERK signaling is a critical regulator of high-risk human papillomavirus oncogene expression revealing therapeutic targets for HPV-induced tumors.PLoS pathogens · 2021Article
- Restoration of tumor suppressor p53 by differentially regulating pro- and anti-p53 networks in HPV-18-infected cervical cancer cells.Oncogene · 2012Article
- Leukemia inhibitory factor downregulates human papillomavirus-16 oncogene expression and inhibits the proliferation of cervical carcinoma cells.Infectious diseases in obstetrics and gynecology · 2011Article
- Two distinct human uterine cervical epithelial cell lines established after transfection with human papillomavirus 16 DNA.Japanese journal of cancer research : Gann · 1997Article
- Article
- Keratinocyte growth factor is a bifunctional regulator of HPV16 DNA-immortalized cervical epithelial cells.The Journal of cell biology · 1995Article
- Transcriptional silencer of the human papillomavirus type 8 late promoter interacts alternatively with the viral trans activator E2 or with a cellular factor.Journal of virology · 1994Article
- NF-IL6 represses early gene expression of human papillomavirus type 16 through binding to the noncoding region.Journal of virology · 1993Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have found that epidermal growth factor (EGF) elicits negative regulation of human papillomavirus type 16 (HPV-16) E6/E7 at the mRNA level in the HPV-16-immortalized human keratinocyte cell line (PHK160b). This down-regulation of HPV-16 E6/E7 expression was achieved when the cells were stimulated to proliferate with the concomitantly enhanced c-myc expression by EGF in a dose-dependent manner. By using partly synchronized PHK160b cells, negative and positive regulations of the HPV-16 E6/E7 expression was correlated to EGF-linked cell cycle events in this particular human keratinocyte cell line. In order to study transcriptional control mechanisms of the HPV-16 E6/E7, transient expression assays were performed with CAT expression plasmids that the transcription could be directed by the 5'-deleted HPV-16 long control region (LCR) including the virus P97 promoter. We demonstrated that the HPV-16 LCR contained EGF-responsive elements and that a predominant silencer activity was mapped in the proximal 124-bp region (EGFRE) of the LCR. This restricted LCR region had significant influence on HPV-16-homologous promoters in lowering the CAT expression in the presence and absence of EGF. EGFRE was thus considered to be a conditional transcription-controlling element on HPV-16 E6/E7 expression in this EGF-responsive human keratinocyte cell line. This suggests that specific sequences in the LCR play a critical part in the EGF-induced down-regulation of E6/E7 expression at the transcriptional level. Since the results obtained from the transient expression assay agreed with the mode of expression of the endogenous HPV-16 E6/E7, the present study strongly suggests that the transcriptional regulation of the HPV-16 E6/E7 oncogene is mediated by growth-related specific cellular factors interacting with HPV-16 LCR elements.
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