期刊
ONCOGENE
卷 35, 期 23, 页码 2979-2990出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2015.364
关键词
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资金
- Department of Veterans Affairs
- National Institutes of Health [R01AA017972, R01CA164311]
- Canadian Institutes of Health Research [MOP-126056]
- Canada Research Chair Program in Viral Hepatitis/Immunology
- Intramural Research Program of the NIH, National Institute on Aging
B-cell receptor (BCR) signaling is essential for the development of B cells and has a critical role in B-cell neoplasia. Increasing evidence indicates an association between chronic hepatitis C virus (HCV) infection and B-cell lymphoma, however, the mechanisms by which HCV causes B-cell lymphoproliferative disorder are still unclear. Herein, we demonstrate the expression of HCV viral proteins in B cells of HCV-infected patients and show that HCV upregulates BCR signaling in human primary B cells. HCV nonstructural protein NS3/4A interacts with CHK2 and downregulates its activity, modulating HuR posttranscriptional regulation of a network of target mRNAs associated with B-cell lymphoproliferative disorders. Interestingly, the BCR signaling pathway was found to have the largest number of transcripts with increased association with HuR and was upregulated by NS3/4A. Our study reveals a previously unidentified role of NS3/4A in regulation of host BCR signaling during HCV infection, contributing to a better understanding of the molecular mechanisms underlying HCV-associated B-cell lymphoproliferative disorders.
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