Abstract
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising agent for cancer therapy. However, a number of prostate cancer cells exhibit high resistance to TRAIL effect. In this study, we found that Triptolide, a Chinese medicine, significantly sensitizes prostate cancer cells to TRAIL-mediated cellular apoptosis by up-regulating DR5 expression. Triptolide treatment can suppress Akt/Hdm2 signaling pathway, and lead to p53 accumulation, thereby up-regulating DR5 expression. Taken together, all evidences indicate that Triptolide may become a promising therapeutic agent that prevents the progression of prostate cancer.
MeSH terms
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Antineoplastic Agents, Alkylating / pharmacology
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Apoptosis / drug effects*
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Cell Line, Tumor
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Cell Survival / drug effects
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Diterpenes / pharmacology*
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Epoxy Compounds / pharmacology
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Gene Expression Regulation, Neoplastic / drug effects
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Humans
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Male
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Phenanthrenes / pharmacology*
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Prostatic Neoplasms / genetics*
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Prostatic Neoplasms / metabolism*
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Proto-Oncogene Proteins c-akt / metabolism
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Proto-Oncogene Proteins c-mdm2 / metabolism
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Receptors, TNF-Related Apoptosis-Inducing Ligand / genetics*
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Receptors, TNF-Related Apoptosis-Inducing Ligand / metabolism
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Signal Transduction / drug effects
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TNF-Related Apoptosis-Inducing Ligand / pharmacology*
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Tumor Suppressor Protein p53 / metabolism*
Substances
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Antineoplastic Agents, Alkylating
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Diterpenes
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Epoxy Compounds
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Phenanthrenes
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Receptors, TNF-Related Apoptosis-Inducing Ligand
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TNF-Related Apoptosis-Inducing Ligand
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Tumor Suppressor Protein p53
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triptolide
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Proto-Oncogene Proteins c-mdm2
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Proto-Oncogene Proteins c-akt