Epstein-Barr virus-encoded latent membrane protein 1 induces epithelial to mesenchymal transition by inducing V-set Ig domain containing 4 (VSIG4) expression via NF-kB in renal tubular epithelial HK-2 cells
- Department of Anatomy and Tumor Immunology, Inje University College of Medicine, 75 Bokji-ro, Busanjin-gu, Pusan 47392 (Korea, Republic of)
- Division of Nephrology, Department of Internal Medicine, Inje University College of Medicine, Ilsan-Paik Hospital, Joowha-ro 170, Ilsan-seo gu, Goyang 10380 (Korea, Republic of)
- Department of Urology, Inje University Haeundae Paik Hospital, 875 Haeundae-ro, Haeundae-gu, Busan 48108 (Korea, Republic of)
The epithelial to mesenchymal transition (EMT), a hallmark of chronic kidney disease, is a key event in the conversion from tubular epithelial cells to myofibroblasts in renal fibrosis. Epstein-Barr virus (EBV) is a γ-herpes oncovirus associated with chronic kidney disease. However, the relationship between EBV and the EMT process in renal tubular epithelial cells is not well understood. Among EBV-latent genes, EBV-encoded latent membrane protein 1 (LMP1) induces EMT by regulating a variety of molecules in EBV-induced oncogenic transformation. In this study, we investigated EBV-encoded LMP1 and EMT process markers in human proximal tubule epithelial cell line HK-2. LMP1 overexpression induces cell morphological changes via the epithelial to mesenchymal process in HK-2 cells, and these changes accelerate cell proliferation, cell motility, and invasion. Furthermore, VSIG4 upregulation by EBV-LMP1 induced LMP1-mediated EMT, cell motility, and invasion. VSIG4 upregulation by LMP1 was regulated at the transcriptional level via the NF-kB signaling axis. These results suggest that EBV-encoded LMP1 regulates EMT through the NF-kB-VSIG4 axis in HK-2 cells, and VSIG4 is a potential target in EBV-induced chronic kidney diseases. - Highlights: • Epstein Barr virus-encoded LMP1 overexpression induces epithelial to mesenchymal transition in renal epithelial HK-2 cells. • Upregulation of VISG4 expression by EBV-LMP1 plays an important role in LMP1-induced EMT process in HK-2 cells. • VSIG4 upregulation by EBV-LMP1 is regulated at transcriptional level via LMP1-induced NF-kB activation. • The interruption of VSIG4 expression could be a potential strategy for treatment of EBV-infected renal diseases.
- OSTI ID:
- 22719108
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 492, Issue 3; Other Information: Copyright (c) 2017 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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