Abstract
Triptolide showed excellent antitumor activity against several solid tumors. However, its mechanism has not been fully understood. To further elucidate it, the effects of mitogen activated protein kinases (MAPKs) on the activity of triptolide towards prostate cancer cell lines were investigated in the present study using both LNCaP (p53 positive and androgen-dependent) and PC-3 (p53 deficient and androgen-independent) cells. Our results showed that triptolide exerted potent growth inhibitory and apoptotic effects on both cell lines, and the effects were independent of the expression of p53. Although upregulation of ERK and JNK phosphorylation was observed after the triptolide treatment, the results with inhibitors showed that these MAPKs were not involved in the mechanism of triptolide activity in human prostate cancer cell lines with different p53 status.
© Georg Thieme Verlag KG Stuttgart · New York.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antineoplastic Agents, Alkylating / pharmacology*
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Antineoplastic Agents, Alkylating / therapeutic use
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Apoptosis / drug effects*
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Cell Line, Tumor
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Cytostatic Agents / pharmacology*
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Cytostatic Agents / therapeutic use
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Diterpenes / pharmacology*
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Diterpenes / therapeutic use
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Epoxy Compounds / pharmacology
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Epoxy Compounds / therapeutic use
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Humans
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MAP Kinase Signaling System
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Male
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Mitogen-Activated Protein Kinases / antagonists & inhibitors
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Mitogen-Activated Protein Kinases / physiology*
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Phenanthrenes / pharmacology*
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Phenanthrenes / therapeutic use
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Prostatic Neoplasms / drug therapy*
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Prostatic Neoplasms / enzymology
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Prostatic Neoplasms / pathology
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Protein Kinase Inhibitors / pharmacology
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Tumor Suppressor Protein p53 / metabolism*
Substances
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Antineoplastic Agents, Alkylating
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Cytostatic Agents
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Diterpenes
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Epoxy Compounds
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Phenanthrenes
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Protein Kinase Inhibitors
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Tumor Suppressor Protein p53
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triptolide
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Mitogen-Activated Protein Kinases