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2017 | 64 | 1 | 35-39
Article title

HBx and SP1 upregulate DKK1 expression

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EN
Abstracts
EN
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
EN
HCC   HBV   DKK1   SP1  
Publisher

Year
Volume
64
Issue
1
Pages
35-39
Physical description
Dates
published
2017
received
2016-01-14
revised
2016-05-20
accepted
2016-07-13
(unknown)
2016-10-10
Contributors
author
  • 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
author
  • Department of forensic medicine, Chongqing Medical University, Chongqing, 400016, China
author
  • Department of forensic medicine, Chongqing Medical University, Chongqing, 400016, China
author
  • 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
author
  • 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
author
  • 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
author
  • 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
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Document Type
Publication order reference
Identifiers
YADDA identifier
bwmeta1.element.bwnjournal-article-abpv64p35kz
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