Authors: Nivedita Gaur Jaya Gandhi Erle S Robertson Subhash C Verma Rajeev Kaul
Publish Date: 2014/12/13
Volume: 36, Issue: 4, Pages: 3051-3060
Abstract
Epithelial–mesenchymal transition is an important mechanism in cancer invasiveness and metastasis We had previously reported that cancer cells expressing Epstein–Barr virus EBV latent viral antigens EBV nuclear antigen EBNA3C and/ or EBNA1 showed higher motility and migration potential and had a propensity for increased metastases when tested in nude mice model We now show that both EBNA3C and EBNA1 can modulate cellular pathways critical for epithelial to mesenchymal transition of cancer cells Our data confirms that presence of EBNA3C or EBNA1 result in upregulation of transcriptional repressor Slug and Snail upregulation of intermediate filament of mesenchymal origin vimentin upregulation of transcription factor TCF8/ZEB1 downregulation as well as disruption of tight junction zona occludens protein ZO1 downregulation of cell adhesion molecule Ecadherin and nuclear translocation of βcatenin We further show that the primary tumors as well as metastasized lesions derived from EBV antigenexpressing cancer cells in nude mice model display EMT markers expression pattern suggesting their greater propensity to mesenchymal transitionThis work was supported by grants from the Department of Biotechnology of Government of India BT/PR15109/GBD/27/320/2011 MRP grant from UGC FN411144/2012 RD grant from the University of Delhi NG is project fellow funded by UGC and JG is senior research fellow funded by UGC ESR is a scholar of the Leukemia and Lymphoma Society of America SCV is funded by NIH public health grants CA174459 AI105000 RK is UGC IndoUS Raman research fellow
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