Abstract
The anticancer activities of secalonic acid D separated from the secondary metabolites of the mangrove endophytic fungus No. ZSU44 were investigated in this study. Secalonic acid D showed potent cytotoxicity to HL60 and K562 cells, and the IC(50) values were 0.38 and 0.43 mumol/L, respectively. Annexin V-FITC/PI assay and western blot indicated that secalonic acid D induced apoptosis in HL60 and K562 cells. In addition, secalonic acid D led to cell cycle arrest of G(1) phase related to downregulation of c-Myc. Moreover, our data indicated that downregulation of c-Myc and cell cycle arrest of G(1) phase were caused not by formation of G-quadruplex structures but by activation of GSK-3beta followed by degradation of beta-catenin.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antineoplastic Agents / pharmacology*
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Apoptosis*
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Cell Line, Tumor
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Cell Survival / drug effects
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Cell Survival / physiology
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G1 Phase / drug effects
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G1 Phase / physiology
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Glycogen Synthase Kinase 3 / drug effects
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Glycogen Synthase Kinase 3 / metabolism*
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Glycogen Synthase Kinase 3 beta
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HL-60 Cells
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Humans
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Proto-Oncogene Proteins c-myc / antagonists & inhibitors
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Proto-Oncogene Proteins c-myc / genetics
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Proto-Oncogene Proteins c-myc / metabolism*
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RNA, Small Interfering / metabolism
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Xanthones / pharmacology*
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Xanthones / toxicity
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beta Catenin / antagonists & inhibitors
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beta Catenin / metabolism*
Substances
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Antineoplastic Agents
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MYC protein, human
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Proto-Oncogene Proteins c-myc
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RNA, Small Interfering
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Xanthones
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beta Catenin
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secalonic acid
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GSK3B protein, human
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Glycogen Synthase Kinase 3 beta
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Glycogen Synthase Kinase 3