Source:http://linkedlifedata.com/resource/pubmed/id/17296261
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2007-6-11
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pubmed:abstractText |
The X protein of hepatitis B virus (HBx) is often expressed in human hepatocellular carcinoma (HCC) but its role on tumor growth is not fully clarified. In this study, RNA interference was employed to knockdown HBx expression in Hep3B HCC cells, which naturally express carboxyl-end truncated form of HBx frequently found in HCC tissues. Specific knockdown of HBx strongly inhibited cell growth and tumorigenicity in xenograft model. HBx repression induced apoptosis in Hep3B cells and significantly increased cell sensitivity to cisplatin-induced apoptosis. These results suggest that RNA interference-mediated HBx suppression exerts potent anti-proliferative and chemosensitizing effects in human HCC.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0304-3835
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
8
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pubmed:volume |
253
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
43-52
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:17296261-Apoptosis,
pubmed-meshheading:17296261-Base Sequence,
pubmed-meshheading:17296261-Carcinoma, Hepatocellular,
pubmed-meshheading:17296261-Cell Proliferation,
pubmed-meshheading:17296261-Cisplatin,
pubmed-meshheading:17296261-Humans,
pubmed-meshheading:17296261-Liver Neoplasms,
pubmed-meshheading:17296261-Molecular Sequence Data,
pubmed-meshheading:17296261-RNA Interference,
pubmed-meshheading:17296261-Trans-Activators,
pubmed-meshheading:17296261-Transfection,
pubmed-meshheading:17296261-Tumor Cells, Cultured,
pubmed-meshheading:17296261-Viral Regulatory and Accessory Proteins
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pubmed:year |
2007
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pubmed:articleTitle |
RNA interference targeting HBx suppresses tumor growth and enhances cisplatin chemosensitivity in human hepatocellular carcinoma.
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pubmed:affiliation |
Department of Medicine and Therapeutics, The Chinese University of Hong Kong, Shatin, Hong Kong.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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