EBV(LMP1)-induced metabolic reprogramming inhibits necroptosis through the hypermethylation of the RIP3 promoter
Authors:
Open Access
- 1 January 2019
- journal article
- research article
- Published by Ivyspring International Publisher in Theranostics
- Vol. 9 (9) , 2424-2438
Abstract
EBV infection is a recognized epigenetic driver of carcinogenesis. We previously showed that EBV could protect cancer cells from TNF-induced necroptosis. This study aims to explore the epigenetic mechanisms allowing cancer cells with EBV infection to escape from RIP3-dependent necroptosis.Keywords
This publication has 46 references indexed in Scilit:
- Epstein-Barr virus encoded latent membrane protein 1 suppresses necroptosis through targeting RIPK1/3 ubiquitinationCell Death & Disease, 2018
- EBV based cancer prevention and therapy in nasopharyngeal carcinomanpj Precision Oncology, 2017
- Viruses and the Diversity of Cell DeathAnnual Review of Virology, 2016
- Methylation-dependent loss of RIP3 expression in cancer represses programmed necrosis in response to chemotherapeuticsCell Research, 2015
- Epstein-Barr Virus Turns 50Science, 2014
- Epstein–Barr Virus Infection as an Epigenetic Driver of TumorigenesisCancer Research, 2012
- RIP3, an Energy Metabolism Regulator That Switches TNF-Induced Cell Death from Apoptosis to NecrosisScience, 2009
- Receptor Interacting Protein Kinase-3 Determines Cellular Necrotic Response to TNF-αCell, 2009
- Epigenetics in CancerNew England Journal of Medicine, 2008
- The Epstein–Barr virus oncogene product, latent membrane protein 1, induces the downregulation of E-cadherin gene expression via activation of DNA methyltransferasesProceedings of the National Academy of Sciences, 2002