Wu H.-C.Lin Y.-J.Lee J.-J.Liu Y.-J.Liang S.-T.Peng Y.Chiu Y.-W.Wu C.-W.CHIN-TARNG LIN2022-03-042022-03-0420030023-6837https://www.scopus.com/inward/record.uri?eid=2-s2.0-0038002724&doi=10.1097%2f01.LAB.0000074896.03561.FB&partnerID=40&md5=858fc755c4ccff9db6d65f70d1c9fae7https://scholars.lib.ntu.edu.tw/handle/123456789/596367A membrane invasion culture system was used to study the ability of EBV to enhance invasion and migration of nasopharyngeal carcinoma (NPC) cells. Semi-reverse transcriptase-PCR analysis of matrix proteinases and angiogenic factors from EBV-infected, or EBV-positive (EBV+), cells demonstrated different degrees of elevated gene expression. In our animal model, EBV+ tumors grew faster and larger than EBV-free, or EBV-negative (EBV-), tumors and also had clonal EBV terminal repeat sequences. Double-localization of EBV and certain host proteins in EBV+ tumors and biopsy specimens demonstrated that EBV up-regulates host genes only in cells that express those genes but not in cells that do not express them. Double-localization of EBV and host genes in NPC biopsy specimens all showed EBV-tumor cells expressing those host genes. Our data strongly suggest that EBV infection enhances progression of NPC tumor growth. They do not rule out a role for EBV infection in the induction and early promotion of NPC development. Unidentified factors may also enhance NPC tumor growth independent of the effects of EBV.[SDGs]SDG3angiogenic factor; matrix metalloproteinase; animal model; animal tissue; article; cancer cell culture; carcinoma cell; cell growth; cell invasion; cell migration; cell structure; controlled study; Epstein Barr virus; gene expression; gene expression regulation; human; human cell; long terminal repeat; mouse; nasopharynx carcinoma; nonhuman; priority journal; protein localization; reverse transcription polymerase chain reaction; SCID mouse; solid tumor; tumor growth; tumor promotion; virus carcinogenesis; virus detection; virus genome; virus infectionjournal article10.1097/01.LAB.0000074896.03561.FB128081152-s2.0-0038002724