|Cancer||Cell death||Cell cycle||Cytoskeleton||Exo/endocytosis||Differentiation||Division||Organelles||Signalling||Stem cells||Trafficking|
EBV up-regulates cytochrome c through VDAC1 regulations and decreases the release of cytoplasmic Ca2+ in the NPC cell line
Xuesong Feng, Chi Bun Ching and Wei Ning Chen1
School of Chemical and Biomedical Engineering, Technological University, 62 Nanyang Drive 637459, Singapore
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.
Key words: Ca2+, cytochrome c, Epstein–Barr virus nasopharyngeal carcinoma, ELISA, siRNA inhibition
Abbreviations: Cyto c, cytochrome c, EBV, Epstein–Barr virus, NPC, nasopharyngeal carcinoma, VDAC1, voltage-dependent anion channel protein 1
1To whom correspondence should be addressed (email WNChen@ntu.edu.sg).
Received 24 June 2011/16 February 2012; accepted 13 April 2012
Published online 19 June 2012, doi:10.1042/CBI20110368
© The Author(s) Journal compilation © 2012 International Federation for Cell Biology