ArticleVirchows Archiv : an international journal of pathology2006
Expression of Epstein-Barr virus (EBV)-encoded latent membrane proteins and STAT3 activation in nasopharyngeal carcinoma.
Article in Virchows Archiv : an international journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Monoamine oxidase A is down-regulated in EBV-associated nasopharyngeal carcinoma.Scientific reports · 2020Article
- Epstein-Barr Virus Hijacks DNA Damage Response Transducers to Orchestrate Its Life Cycle.Viruses · 2017Review
- A Central Role for STAT3 in Gammaherpesvirus-Life Cycle and -Diseases.Frontiers in microbiology · 2016Review
- SYK interaction with ITGβ4 suppressed by Epstein-Barr virus LMP2A modulates migration and invasion of nasopharyngeal carcinoma cells.Oncogene · 2015Article
- Article
- c-Myc and EBV-LMP1: two opposing regulators of the HLA class I antigen presentation machinery in epithelial cells.British journal of cancer · 2012Article
- Epstein-Barr virus LMP1 activates EGFR, STAT3, and ERK through effects on PKCdelta.Journal of virology · 2011Article
- Molecular parameters of head and neck cancer metastasis.Critical reviews in eukaryotic gene expression · 2011Review
- Epstein-Barr virus latent membrane protein 1 induces expression of the epidermal growth factor receptor through effects on Bcl-3 and STAT3.Journal of virology · 2008Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Epstein-Barr virus (EBV) is associated with virtually all cases of undifferentiated nasopharyngeal carcinoma (NPC), and it was proposed that the EBV-encoded transforming protein, latent membrane protein (LMP) 1, may play a role in the neoplastic process. It was proposed recently that LMP1 expression in epithelial cells may be regulated through a loop involving activated signal transducer and activator of transcription 3 (STAT3), LMP1, LMP1-mediated induction of interleukin (IL)-6 expression and STAT3 activation through the IL-6 receptor. This autoregulatory loop may be suppressed by another viral protein, LMP2A, an effect which in turn can be overcome by exogenous IL-6. Here we show that, as expected, expression of LMP1 and LMP2A tend to be exclusive in NPC tumours. Rare cases showing a co-expression of both proteins can be explained by STAT3 activation via the receptors for IL-6 or epidermal growth factor. STAT3 activation was a consistent feature of NPC tumour cells. However, in most cases, this was not accompanied by detectable expression of LMP1, suggesting either that LMP2A expression may suffice to suppress LMP1 expression or that additional factors may be operational. This study emphasises the need to correlate in vitro results with observational studies of ex vivo tumour tissues.
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