title: Association between Epstein-Barr virus infection and chemoresistance to docetaxel in gastric carcinoma.
abstract: Epstein-Barr virus (EBV) is associated with human cancers such as nasopharyngeal carcinoma, Burkitt's lymphoma, Hodgkin's disease, and gastric carcinoma (GC). EBV is associated with about 10% of all GC cases globally. EBV-associated GC has distinct features from EBV-negative GC. However, it is still unclear if EBV infection has any effect on GC chemoresistance. Cell proliferation assay, cell cycle analysis, and active caspase Western blot revealed that the EBV-positive GC cell line (AGS-EBV) showed chemoresistance to docetaxel compared to the EBV-negative GC cell line (AGS). Docetaxel treatment increased expression of Bax similarly in AGS and AGS-EBV cell lines. However, Bcl-2 induction was markedly higher in AGS-EBV cells, after docetaxel treatment. Although docetaxel increased the expression of p53 to a similar extent in both cell lines, induction of p21 in AGS-EBV cells was lower than in AGS cells. Furthermore, expression of survivin was higher in AGS-EBV cells than in AGS cells following docetaxel treatment as well as at basal state. EBVlytic gene expression was induced by docetaxel treatment in AGS-EBV cells. The results suggest that EBV infection and lytic induction confers chemoresistance to GC, possibly by regulating cellular and EBV latent and lytic gene expression.
authors.affiliation: Research Institute of Immunobiology, Department of Medical Lifescience, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea.
authors.forename: Hee Jong
authors.initials: HJ
authors.lastname: Shin
authors.forename: Do Nyun
authors.initials: DN
authors.lastname: Kim
authors.forename: Suk Kyeong
authors.initials: SK
authors.lastname: Lee
mesh_terms: D002277:Carcinoma / Q000188:drug therapy* / Q000473:pathology / Q000821:virology; D002461:Cell Line, Transformed; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000235:genetics / Q000378:metabolism; D000077143:Docetaxel; D019008:Drug Resistance, Neoplasm; D020031:Epstein-Barr Virus Infections / Q000188:drug therapy* / Q000473:pathology / Q000821:virology; D015967:Gene Expression Regulation, Viral / Q000187:drug effects; D004854:Herpesvirus 4, Human / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D051034:Inhibitor of Apoptosis Proteins / Q000235:genetics / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism; D013274:Stomach Neoplasms / Q000188:drug therapy* / Q000473:pathology / Q000821:virology; D000077022:Survivin; D043823:Taxoids / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: C107489:BIRC5 protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D051034:Inhibitor of Apoptosis Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D000077022:Survivin; D043823:Taxoids; D000077143:Docetaxel