title: EBV up-regulates cytochrome c through VDAC1 regulations and decreases the release of cytoplasmic Ca2+ in the NPC cell line.
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.
authors.affiliation: School of Chemical and Biomedical Engineering, Technological University, 62 Nanyang Drive 637459, Singapore.
authors.forename: Xuesong
authors.initials: X
authors.lastname: Feng
authors.forename: Chi Bun
authors.initials: CB
authors.lastname: Ching
authors.forename: Wei Ning
authors.initials: WN
authors.lastname: Chen
mesh_terms: D002118:Calcium / Q000378:metabolism*; D002277:Carcinoma; D045744:Cell Line, Tumor; D045304:Cytochromes c / Q000378:metabolism*; D003593:Cytoplasm / Q000378:metabolism; D020031:Epstein-Barr Virus Infections / Q000378:metabolism* / Q000473:pathology / Q000821:virology; D004854:Herpesvirus 4, Human / Q000378:metabolism*; D006801:Humans; D007477:Ions / Q000737:chemistry; D000077274:Nasopharyngeal Carcinoma; D009303:Nasopharyngeal Neoplasms / Q000378:metabolism / Q000473:pathology; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000378:metabolism; D015398:Signal Transduction; D015854:Up-Regulation; D050995:Voltage-Dependent Anion Channel 1 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*
chemical_list: D007477:Ions; D034741:RNA, Small Interfering; C494762:VDAC1 protein, human; D045304:Cytochromes c; D050995:Voltage-Dependent Anion Channel 1; D002118:Calcium