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Acta Biochim Pol. 2017;64(1):35-39. doi: 10.18388/abp.2016_1250. Epub 2016 Oct 10.

HBx and SP1 upregulate DKK1 expression.

Author information

1
Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Institute for Viral Hepatitis, Department of Infectious Diseases, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, PR China.
2
Department of forensic medicine, Chongqing Medical University, Chongqing, 400016, China.

Abstract

Numerous evidences suggested that the hepatitis B virus (HBV) was recognized as an important factor in the development of hepatocellular carcinoma (HCC). Dickkopf-1 (DKK1) recently was reported to be involved in the progress of HCC. HBV may regulate DKK1 expression in hematoma carcinogenesis. Here, we demonstrated that HBV could regulate DKK1 promoter activity which resulted in upregulation of its mRNA and protein expression in several HBV existing cell lines, and HBx played a prominent role in this process. Transcription factor binding site search result showed that there is a SP1 site in DKK1 promoter region. Luciferase assay showed that overexpression of SP1 could increase DKK1 promoter activity in a dose dependent manner. Accordingly, siRNA inhibition of SP1 expression reduced DKK1 promoter activity and decreased the expression of DKK1 protein.

KEYWORDS:

DKK1; HBV; HCC; SP1

PMID:
27723845
DOI:
10.18388/abp.2016_1250
[Indexed for MEDLINE]
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