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

Seung Mi Kim; Se Won Oh; Sang Hyun Park; Dae Young Hur; Seung Woo Hong; Sang Youb Han

doi:10.1016/j.bbrc.2017.08.116

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

Seung Mi Kim, Se Won Oh, Sang Hyun Park, Dae Young Hur, Seung Woo Hong, Sang Youb Han

Research output: Contribution to journal › Article › peer-review

7 Citations (Scopus)

Abstract

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.

Original language	English
Pages (from-to)	316-322
Number of pages	7
Journal	Biochemical and biophysical research communications
Volume	492
Issue number	3
DOIs	https://doi.org/10.1016/j.bbrc.2017.08.116
Publication status	Published - 2017 Oct 21
Externally published	Yes

Keywords

EBV
EMT
LMP1
NF-kB
Renal tubular cell
VSIG4

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.bbrc.2017.08.116

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Kim, S. M., Oh, S. W., Park, S. H., Hur, D. Y., Hong, S. W., & Han, S. Y. (2017). 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. Biochemical and biophysical research communications, 492(3), 316-322. https://doi.org/10.1016/j.bbrc.2017.08.116

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. / Kim, Seung Mi; Oh, Se Won; Park, Sang Hyun et al.
In: Biochemical and biophysical research communications, Vol. 492, No. 3, 21.10.2017, p. 316-322.

Research output: Contribution to journal › Article › peer-review

Kim, SM, Oh, SW, Park, SH, Hur, DY, Hong, SW & Han, SY 2017, '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', Biochemical and biophysical research communications, vol. 492, no. 3, pp. 316-322. https://doi.org/10.1016/j.bbrc.2017.08.116

Kim SM, Oh SW, Park SH, Hur DY, Hong SW, Han SY. 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. Biochemical and biophysical research communications. 2017 Oct 21;492(3):316-322. doi: 10.1016/j.bbrc.2017.08.116

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abstract = "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.",

keywords = "EBV, EMT, LMP1, NF-kB, Renal tubular cell, VSIG4",

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