Abstract
Cucurbitacin B is an anti-cancer drug candidate and its efficacy has been demonstrated in hepatocellular carcinoma (HCC). To explore its mechanism against HCC, BEL-7402 cells were treated with cucurbitacin B in vitro. Treatment with cucurbitacin B induced S phase arrest and apoptosis. The growth inhibition effect was associated with cyclin D1 and cdc-2 down regulations. Western blotting analysis of cell signaling molecules indicated that cucurbitacin B inhibited c-Raf activation without affecting STAT3 phosphorylation. Moreover, in vivo study demonstrated that cucurbitacin B is effective against BEL-7402 xenograft when administrated orally.
Copyright (c) 2010 Elsevier Ireland Ltd. All rights reserved.
MeSH terms
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Administration, Oral
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Animals
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Antineoplastic Agents / pharmacology
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Antineoplastic Agents / therapeutic use*
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Apoptosis / drug effects*
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Blotting, Western
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Carcinoma, Hepatocellular / drug therapy
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Carcinoma, Hepatocellular / pathology*
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Cell Cycle / drug effects*
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Cell Division / drug effects
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Cell Line, Tumor
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Flow Cytometry
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Humans
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Liver Neoplasms / drug therapy
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Liver Neoplasms / pathology*
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Mice
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Mice, Nude
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Proto-Oncogene Proteins c-raf / metabolism
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S Phase / drug effects*
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STAT3 Transcription Factor / drug effects
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STAT3 Transcription Factor / metabolism
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Transplantation, Heterologous
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Triterpenes / pharmacology*
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Triterpenes / therapeutic use*
Substances
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Antineoplastic Agents
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STAT3 Transcription Factor
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Triterpenes
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cucurbitacin C
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Proto-Oncogene Proteins c-raf