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Decoy receptor 3, upregulated by Epstein-Barr virus latent membrane protein 1, enhances nasopharyngeal carcinoma cell migration and invasion.
Carcinogenesis. 2009 Aug; 30(8):1443-51.C

Abstract

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.

Authors+Show Affiliations

Institute of Microbiology and Immunology, National Yang-Ming University, No. 155, Section 2, Linong Street, Taipei 112, Taiwan.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19483191

Citation

Ho, Cheng-Hsun, et al. "Decoy Receptor 3, Upregulated By Epstein-Barr Virus Latent Membrane Protein 1, Enhances Nasopharyngeal Carcinoma Cell Migration and Invasion." Carcinogenesis, vol. 30, no. 8, 2009, pp. 1443-51.
Ho CH, Chen CL, Li WY, et al. Decoy receptor 3, upregulated by Epstein-Barr virus latent membrane protein 1, enhances nasopharyngeal carcinoma cell migration and invasion. Carcinogenesis. 2009;30(8):1443-51.
Ho, C. H., Chen, C. L., Li, W. Y., & Chen, C. J. (2009). Decoy receptor 3, upregulated by Epstein-Barr virus latent membrane protein 1, enhances nasopharyngeal carcinoma cell migration and invasion. Carcinogenesis, 30(8), 1443-51. https://doi.org/10.1093/carcin/bgp135
Ho CH, et al. Decoy Receptor 3, Upregulated By Epstein-Barr Virus Latent Membrane Protein 1, Enhances Nasopharyngeal Carcinoma Cell Migration and Invasion. Carcinogenesis. 2009;30(8):1443-51. PubMed PMID: 19483191.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Decoy receptor 3, upregulated by Epstein-Barr virus latent membrane protein 1, enhances nasopharyngeal carcinoma cell migration and invasion. AU - Ho,Cheng-Hsun, AU - Chen,Chi-Long, AU - Li,Wing-Yin, AU - Chen,Chi-Ju, Y1 - 2009/05/29/ PY - 2009/6/2/entrez PY - 2009/6/2/pubmed PY - 2009/9/2/medline SP - 1443 EP - 51 JF - Carcinogenesis JO - Carcinogenesis VL - 30 IS - 8 N2 - 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. SN - 1460-2180 UR - https://www.unboundmedicine.com/medline/citation/19483191/Decoy_receptor_3_upregulated_by_Epstein_Barr_virus_latent_membrane_protein_1_enhances_nasopharyngeal_carcinoma_cell_migration_and_invasion_ L2 - https://academic.oup.com/carcin/article-lookup/doi/10.1093/carcin/bgp135 DB - PRIME DP - Unbound Medicine ER -