Peroxisome-localized hepatitis Bx protein increases the invasion property of hepatocellular carcinoma cells
HBx acts as a multifunctional regulator that modulates various cellular responses, which can lead to development and progression of hepatocellular carcinoma (HCC). Here, we show that the HBx protein is also localized to peroxisomes, and this increases cellular reactive oxygen species (ROS) to levels that are higher than when HBx is localized to other organelles. The elevated ROS strongly activated nuclear factor (NF)-κB. In addition, the peroxisome-localized HBx increased the expressions of matrix metalloproteinases and decreased the expression of E-cadherin, which increased the invasive ability of HCC cells. Thus, a specific distribution of HBx to peroxisomes may contribute to HCC progression by increasing the invasive ability of HCC cells through elevation of the cellular ROS level.
KeywordsGreen Fluorescent Protein HepG2 Cell Reactive Oxygen Species Level Hep3B Cell Quantitative Reverse Transcription Polymerase Chain
Hepatitis B virus
Nuclear factor κB
Reactive oxygen species
Mitochondrial fission 1 protein
Dulbecco’s modified Eagle’s medium
Fetal bovine serum
Sodium dodecyl sulfate
Internal ribosome entry site
Green fluorescent protein
Reverse transcription polymerase chain reaction
Mitochondrial antiviral signaling
Peroxisomal biogenesis factor 5
This work was supported by a grant of the Korean Health Technology R&D Project, Ministry of Health & Welfare, Republic of Korea (A111838) and by the National Research Foundation of Korea (NRF), funded by the Ministry of Education, Science and Technology (MEST)(NRF-2013R1A1A2010995).
Conflict of interest
We confirm that all authors fulfill all conditions required for authorship. We also confirm that there is no potential conflict of interest or financial dependence regarding this publication, as described in the Instructions for Authors. All authors have read and approved the manuscript.