[Hepatitis B virus X protein upregulates the transcription activity of zinc finger transcription factor SNAI1].

OBJECTIVE

To investigate whether Hepatitis B virus X protein (HBx) regulates the transcription activity of zinc finger transcription factor SNAI1, and to define the main regulation domain.

METHODS

A series of 5' truncated promoters of SNAI1 were amplified and subcloned into the pGL3-Basic vector to construct promoter luciferase report plasmids. The promoter luciferase report plasmids were cotransfected with HBx recombinant adenovirus and pRL-TK plasmid into human hepatocellular cancer cells of the line SMMC7721. Luciferase activity was measured, and relative luciferase activity was calculated.

RESULTS

Luciferase reporter plasmids containing 5' flanking deletion of SNAI1 promoter were successfully constructed. HBx obviously upregulated the activity of the SNAI1 promoter (-869 - +59), other than the SNAI1 promoter (-514 - +59) and SNAI1 promoter (-194 - +59).

CONCLUSION

HBx can stimulate the transcription of SNAI1, and the transcription regulation domain is located in the segment from -869 - -514 of the SNAI1 promoter.