Abstract
Apoptosis, the cell's natural mechanism for death, is a promising target for anticancer therapy. Both the intrinsic and extrinsic pathways use caspases to carry out apoptosis through the cleavage of hundreds of proteins. In cancer, the apoptotic pathway is typically inhibited through a wide variety of means including overexpression of antiapoptotic proteins and under-expression of proapoptotic proteins. Many of these changes cause intrinsic resistance to the most common anticancer therapy, chemotherapy. Promising new anticancer therapies are plant-derived compounds that exhibit anticancer activity through activating the apoptotic pathway.
Keywords:
anticancer therapy; apoptosis; apoptotic evasion; curcumin.
MeSH terms
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Animals
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Antineoplastic Agents, Phytogenic / pharmacology*
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Apoptosis / drug effects
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Carcinogenesis / drug effects
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Carcinogenesis / genetics
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Carcinogenesis / metabolism
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Carcinogenesis / pathology
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Caspases / genetics*
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Caspases / metabolism
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Cell Line, Tumor
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Curcumin / pharmacology*
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Fas Ligand Protein / genetics
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Fas Ligand Protein / metabolism
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Gene Expression Regulation, Neoplastic*
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Humans
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Mice
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Molecular Targeted Therapy*
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Neoplasms / drug therapy*
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Neoplasms / genetics
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Neoplasms / metabolism
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Neoplasms / pathology
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Proto-Oncogene Proteins c-bcl-2 / genetics
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Proto-Oncogene Proteins c-bcl-2 / metabolism
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Signal Transduction
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bcl-2-Associated X Protein / genetics
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bcl-2-Associated X Protein / metabolism
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fas Receptor / genetics
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fas Receptor / metabolism
Substances
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Antineoplastic Agents, Phytogenic
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BAX protein, human
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BCL2 protein, human
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FAS protein, human
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FASLG protein, human
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Fas Ligand Protein
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Proto-Oncogene Proteins c-bcl-2
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bcl-2-Associated X Protein
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fas Receptor
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Caspases
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Curcumin