Open AccessHBx and SP1 upregulate DKK1 expression.
Author(s) -
Hong Peng,
Yongguo Li,
Yunzhi Liu,
Jingnan Zhang,
Ke Chen,
Ailong Huang,
Hua Tang
Publication year - 1970
Publication title -
acta biochimica polonica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.452
H-Index - 78
eISSN - 1734-154X
pISSN - 0001-527X
DOI - 10.18388/abp.2016_1250
Subject(s) - dkk1 , hbx , downregulation and upregulation , sp1 transcription factor , luciferase , hepatitis b virus , cancer research , transcription factor , carcinogenesis , microbiology and biotechnology , chemistry , transcription (linguistics) , messenger rna , promoter , biology , gene expression , gene , transfection , virology , virus , biochemistry , wnt signaling pathway , linguistics , philosophy
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.
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