Abstract
NF-B (Nuclear Factor Kappa B) is a crucial transcription factor that is essential for host survival during pathogen infection in animal and human. Therefore, it has been a main goal for numerous pathogens to modify cellular NF-κB activity to create an environment conducive to their survival within the host. In the present study, the cell line type (SW480) was used as a model of colon cancer cells. Subsequently and through using western blotting, the effect of ORF3 protein on TNF- induced NF-B activation was observed by detecting the NF-B p65 subunit in the nuclear and cytoplasmic extracts. The results appeared that p65 translocated into the nucleus when stimulated by TNF-α in the control groups (GFP and mock cells). However, weak nuclear translocation was seen in ORF3-expressing cells. Moreover, the experiment revealed the ORF3 protein in SW480 inhibited the nuclear translocation of the p65 protein. After TNF-α stimulation, the difference in the band intensity of NF-κB protein in the nuclear fraction of control groups cells from each GFP group (A3) and mock cells (B3) was significantly higher compared with nuclear extract from Orf3expressed cells (C3 , P = 0.0001). In conclusion, the current study was confirmed that HEV ORF3 protein inhibits the activity of cellular NF-κB in human colon cancer cells.
Keywords
activity
Hepatitis E virus
HEV