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Proteome analysis of the transformation potential of the Epstein–Barr virus-encoded latent membrane protein 1 in nasopharyngeal epithelial cells NP69

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Abstract

Latent membrane protein 1 (LMP1) of Epstein–Barr virus has been identified to be crucial in inducing cell transformation. However, the mechanism of LMP1-mediated epithelial cell transformation remains unclear. In this study, nasopharyngeal epithelial cells NP69 were infected with retrovirus with gene encoding wild type LMP1 or mutational LMP1 defective in binding to tumor necrosis factor receptor-associated death domain (TRADD). The NP69-LMP1TRADD lost some malignant phenotypes compared with the NP69-LMP1WT. We performed proteomic approach to gain the differential protein expression profile associated with LMP1-mediated epithelial cell transformation. Furthermore, the differential expressional levels of partial identified proteins were confirmed by Western blot and real-time RT-PCR. Some were known to be related to the development of LMP1-induced transformation, and some were new LMP1-associated proteins. These data are valuable for further study of the mechanism of LMP1 in human nasopharyngeal carcinoma and provide some new clues for investigating other LMP1-associated tumors.

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Abbreviations

2-DE:

Two-dimensional gel electrophoresis

EBV:

Epstein–Barr virus

LMP1:

Latent membrane protein 1

NPC:

Nasopharyngeal carcinoma

TRADD:

Tumor necrosis factor receptor-associated death domain

WT:

Wild type

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Acknowledgments

We thank Dr. Sai Wah Tsao (Hong Kong University) for kindly providing NP69 cells and Dr. Liang Cao for S12 antibody. Grant sponsor: the National Science Foundation of China; grant number: 30470668.

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Correspondence to Zhimin He.

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Qiong Zhang and Zhiwei Zhang contributed equally to this work.

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Zhang, Q., Zhang, Z., Wang, C. et al. Proteome analysis of the transformation potential of the Epstein–Barr virus-encoded latent membrane protein 1 in nasopharyngeal epithelial cells NP69. Mol Cell Biochem 314, 73–83 (2008). https://doi.org/10.1007/s11010-008-9767-8

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  • DOI: https://doi.org/10.1007/s11010-008-9767-8

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