HBx co-localizes with COXIII in HL-7702 cells to upregulate mitochondrial function and ROS generation
Abstract
Hepatocellular carcinoma (HCC) is one of the most common malignant diseases, and HBx leads to the development of HBV-associated HCC. Mitochondria are key organelles that regulate apoptosis, cellular energetics and signal transduction pathways, and are the source of HBx-induced reactive oxygen species (ROS). Recent findings have shown that HBx interacts with the inner mitochondrial membrane protein, COXIII, via the yeast two-hybrid system, mating experiment and coimmunoprecipitation. The aim of the present study was to examine the co-localizaiton of HBx and COXIII in HL-7702 cells and to investigate ensuing alterations of mitochondrial function. An HL-7702 cell line stably expressing the HBx gene by lentivirus vectors was constructed. Confocal microscopy was utilized to assess the interaction between HBx protein and COXIII. Expression of COXIII, activities of cytochrome c oxidase (COX) and the mitochondrial membrane potential, which were functionally relevant to the HBx protein-COXIII interaction, were investigated in cell cultures. Moreover, the intracellular ROS levels were detected by flow cytometry. The results demonstrated that HBx co-localized with the inner mitochondrial protein, COXIII, in HL-7702 cells, causing the upre...Continue Reading
References
Human hepatitis B virus-X protein alters mitochondrial function and physiology in human liver cells.
Hepatitis B virus X protein stimulates the mitochondrial translocation of Raf-1 via oxidative stress
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