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EBV up-regulates cytochrome c through VDAC1 regulations and decreases the release of cytoplasmic Ca2+ in the NPC cell line

Authors

  • Xuesong Feng,

    1. School of Chemical and Biomedical Engineering, Technological University, 62 Nanyang Drive 637459, Singapore
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  • Chi Bun Ching,

    1. School of Chemical and Biomedical Engineering, Technological University, 62 Nanyang Drive 637459, Singapore
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  • Wei Ning Chen

    Corresponding author
    1. School of Chemical and Biomedical Engineering, Technological University, 62 Nanyang Drive 637459, Singapore
      To whom correspondence should be addressed (email WNChen@ntu.edu.sg).
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To whom correspondence should be addressed (email WNChen@ntu.edu.sg).

Abstract

EBV (Epstein—Barr virus) is considered to be a major factor that causes NPC (nasopharyngeal carcinoma), which is one of the sneakiest cancers frequently occurring in Southeast Asia and Southern China. Apoptosis and pro-apoptotic signals have been studied for decades; however, few have extended the prevailing view of EBV to its impact on NPC in perspective of apoptosis. One of the important proteins named VDAC1 (voltage-dependent anion protein 1) on the mitochondrial outer membrane controls the pro-apoptotic signals in mammalian cells. The impact of EBV infection on VDAC1 and related apoptotic signals remains unclear. In order to study the VDAC1′s role in EBV-infected NPC cells, we employ siRNA (small interfering RNA) inhibition to analyse the release of Ca2+ and Cyto c (cytochrome c) signals in the cytoplasm, as they are important pro-apoptotic signals. The results show a decrease of Ca2+ release and up-regulation of Cyto c with EBV infection. After siRNA transfection, the dysregulation of Cyto c is neutralized, which is evidence that the level of Cyto c release in virus-infected NPC cells is the as same as that of non-infected NPC cells. This result indicates that EBV infection changes the cytoplasmic level of Cyto c through regulating VDAC1. In summary, this study reports that EBV changes the release of Ca2+ and Cyto c in the cytoplasm of NPC cells, and that Cyto c changes are mediated by VDAC1 regulation.

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