Document Detail


Anthracenedione derivative 1403P-3 induces apoptosis in KB and KBv200 cells via reactive oxygen species-independent mitochondrial pathway and death receptor pathway.
MedLine Citation:
PMID:  17786034     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Anthracenedione derivatives are potent cytotoxic agents to tumor cells. In this study, we investigated the anticancer activities of anthracenedione derivative 1403P-3 separated from the secondary metabolites of the mangrove endophytic fungus No. 1403. Our results demonstrated that 1403P-3 showed potent cytotoxicity not only to human epidermoid carcinoma drug-sensitive parental KB cells but also to multidrug resistant (MDR) KBv200 cells and the IC50 values were 19.66 and 19.27 muM, respectively. Further research indicated that 1403P-3 induced apoptosis in KB cells and KBv200 cells confirmed by Hoechst 33258 staining, detection of DNA fragmentation and cleavage of poly (ADP-ribose) polymerase (PARP). Furthermore, apoptosis triggered by 1403P-3 was characterized by the loss of mitochondrial membrane potential (DeltaPsi(m)), release of cytochrome c, cleavage of Bid, and activation of caspases-2, -3, -7, -8 and -9. Z-IETD-FMK, caspase-8 inhibitor could inhibit the activation of caspase-2 and cleavage of Bid induced by 1403P-3. However, activation of caspase-9 and cleavage of PARP caused by 1403P-3 were not inhibited by Z-IETD-FMK. Additionally, 1403P-3 did not influence the expression level of Bcl-2 and Bax. It is noteworthy that 1403P-3 decreased the generation of reactive oxygen species (ROS) in KB cells and KBv200 cells. DNA binding assay exhibited that apoptosis induced by 1403P-3 was not involved in intercalating to DNA. In summary, 1403P-3 induced apoptosis of KB cells and KBv200 cells through mitochondrial pathway and death receptor pathway. Furthermore, the mitochondrial pathway was independent of reactive oxygen species and activation of caspase-8.
Authors:
Jian-ye Zhang; Hai-ying Wu; Xue-kui Xia; Yong-ju Liang; Yan-yan Yan; Zhi-gang She; Yong-cheng Lin; Li-wu Fu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-06-05
Journal Detail:
Title:  Cancer biology & therapy     Volume:  6     ISSN:  1555-8576     ISO Abbreviation:  Cancer Biol. Ther.     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2008-01-11     Completed Date:  2008-05-28     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101137842     Medline TA:  Cancer Biol Ther     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1413-21     Citation Subset:  IM    
Affiliation:
State Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-sen University, Guangzhou, PR, China.
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MeSH Terms
Descriptor/Qualifier:
Anthraquinones / chemistry*,  pharmacology
Apoptosis
BH3 Interacting Domain Death Agonist Protein / metabolism
Caspases / metabolism
Cell Line, Tumor
Cell Survival
DNA Fragmentation
Dose-Response Relationship, Drug
Enzyme Inhibitors / pharmacology
Humans
Membrane Potentials
Mitochondria / metabolism*
Models, Biological
Reactive Oxygen Species*
Receptors, Death Domain / metabolism*
Chemical
Reg. No./Substance:
0/1403P-3 compound; 0/Anthraquinones; 0/BH3 Interacting Domain Death Agonist Protein; 0/Enzyme Inhibitors; 0/Reactive Oxygen Species; 0/Receptors, Death Domain; EC 3.4.22.-/Caspases

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