Abstract
ZBP-89 inhibits the some tumor cells but its role in HCC is unknown. We investigated effect of ZBP-89 on cell death of 5 HCC cell lines with different status of p53. We found that ZBP-89 significantly induced cell death of all HCC cells particularly those with wild-type p53. The inhibition was well correlated with the induction of caspase-6 activity. The inhibition of caspase-6 abolished the effect of ZBP-89. ZBP-89 reduced the cells in G2-M but increased them in S phase. With the changes in caspase-6 and cell cycle, ZBP-89 greatly enhanced the killing effectiveness of 5-fluorouracil or staurosporine in HCC cells.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Antineoplastic Agents / pharmacology
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Carcinoma, Hepatocellular / metabolism*
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Caspase 6 / metabolism*
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Cell Cycle / drug effects
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Cell Cycle / physiology
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Cell Death / drug effects
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Cell Death / physiology
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Cell Line, Tumor
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DNA-Binding Proteins / metabolism*
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Flow Cytometry
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Fluorouracil / pharmacology
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Humans
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Liver Neoplasms / metabolism*
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S Phase / drug effects
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S Phase / physiology*
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Staurosporine / pharmacology
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Transcription Factors / metabolism*
Substances
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Antineoplastic Agents
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DNA-Binding Proteins
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Transcription Factors
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ZNF148 protein, human
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Caspase 6
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Staurosporine
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Fluorouracil