Source:http://linkedlifedata.com/resource/pubmed/id/19483191
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
|
pubmed:dateCreated |
2009-7-30
|
pubmed:abstractText |
Decoy receptor 3 (DcR3), a member of tumor necrosis factor receptor superfamily, has been implicated in tumorigenesis through its abilities to modulate immune responses and induce angiogenesis. Epstein-Barr virus (EBV), a ubiquitous gamma-herpesvirus, is associated with malignancies including nasopharyngeal carcinoma (NPC). Previous studies show that DcR3 is overexpressed in EBV-positive lymphomas and Rta, an EBV transcription activator, can upregulate DcR3 in Burkitt lymphoma cell lines. However, DcR3 expression has not been demonstrated in EBV-associated NPC nor have there been any EBV latent genes linked to DcR3 upregulation. Here, we showed DcR3 was overexpressed in NPC. Higher DcR3 expression score and DcR3-positive rate were found in metastatic NPC than in primary NPC tissues, suggesting DcR3 may enhance cell metastatic potential. This hypothesis is supported by our observation that NPC HONE-1 cells overexpressing DcR3 exhibited significant higher migration and invasion abilities in vitro. We found besides Rta, EBV latent membrane protein (LMP) 1 can upregulate DcR3 via nuclear factor-kappaB and phosphatidylinositol 3-kinase-signaling events. Approximate 75% of LMP1-positive NPC tissues overexpressed DcR3, suggesting LMP1 may enhance DcR3 expression in vivo. Data herein suggested that increasing DcR3 expression by LMP1 not only helps EBV-associated cancer cells gain survival advantage by preventing host immune detection but also increases the chance of cancer metastasis by enhancing cell migration and invasion. All these DcR3-mediated events facilitate normal cells to gain cancer hallmarks.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/EBV-associated membrane antigen...,
http://linkedlifedata.com/resource/pubmed/chemical/Luciferases,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphatidylinositol 3-Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor...,
http://linkedlifedata.com/resource/pubmed/chemical/Viral Matrix Proteins
|
pubmed:status |
MEDLINE
|
pubmed:month |
Aug
|
pubmed:issn |
1460-2180
|
pubmed:author | |
pubmed:issnType |
Electronic
|
pubmed:volume |
30
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1443-51
|
pubmed:dateRevised |
2010-11-18
|
pubmed:meshHeading |
pubmed-meshheading:19483191-Blotting, Western,
pubmed-meshheading:19483191-Cell Movement,
pubmed-meshheading:19483191-Chromatin Immunoprecipitation,
pubmed-meshheading:19483191-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:19483191-Epstein-Barr Virus Infections,
pubmed-meshheading:19483191-Gene Expression Regulation,
pubmed-meshheading:19483191-Herpesvirus 4, Human,
pubmed-meshheading:19483191-Humans,
pubmed-meshheading:19483191-Immunoenzyme Techniques,
pubmed-meshheading:19483191-Luciferases,
pubmed-meshheading:19483191-NF-kappa B,
pubmed-meshheading:19483191-Nasopharyngeal Neoplasms,
pubmed-meshheading:19483191-Neoplasm Invasiveness,
pubmed-meshheading:19483191-Phosphatidylinositol 3-Kinases,
pubmed-meshheading:19483191-RNA, Messenger,
pubmed-meshheading:19483191-Receptors, Tumor Necrosis Factor, Member 6b,
pubmed-meshheading:19483191-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:19483191-Up-Regulation,
pubmed-meshheading:19483191-Viral Matrix Proteins,
pubmed-meshheading:19483191-Virus Latency
|
pubmed:year |
2009
|
pubmed:articleTitle |
Decoy receptor 3, upregulated by Epstein-Barr virus latent membrane protein 1, enhances nasopharyngeal carcinoma cell migration and invasion.
|
pubmed:affiliation |
Institute of Microbiology and Immunology, National Yang-Ming University, No. 155, Section 2, Linong Street, Taipei 112, Taiwan.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|