Inhibition of tumor growth in vitro and in vivo by fucoxanthin against human leukemia HL-60 cells and melanoma B16F10 cells
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Title
- Inhibition of tumor growth in vitro and in vivo by fucoxanthin against human leukemia HL-60 cells and melanoma B16F10 cells
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Author(s)
- 허수진; 예보람; 장지이; 김준성; 김민선; 김지형; 이영득; 이수진; 오철홍; 강도형
- KIOST Author(s)
- Heo, Soo Jin(허수진); Kim, Jun Seong(김준성); Lee, Young Deuk(이영득); Lee, Sujin(이수진); Oh, Chul Hong(오철홍); Kang, Do Hyung(강도형)
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Alternative Author(s)
- 허수진; 예보람; 장지이; 김준성; 김민선; 김지형; 이영득; 이수진; 오철홍; 강도형
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Publication Year
- 2013-07-10
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Abstract
- In the present study, we designed to evaluate the molecular mechanism of fucoxanthin isolated from brown algae against HL-60 and B16F10 cell lines. We found that ROS are generated during fucoxanthin-induced apoptosis in HL-60 cells, and NAC which is a scavenger of ROS, suppressed fucoxantin-induced cytotoxicity and apoptosis. Furthermore, the treatment with NAC dramatically inhibited fucoxanthin-induced phosphorylation of JNK and p38 kinase in HL-60 cells. Moreover, fucoxanthin reduced the viability of B16F10 cells in a dose-dependent manner accompanied by the induction of cell cycle arrest during the G0/G1 phase and apoptosis. Fucoxanthin-induced G0/G1 arrest was associated with a marked decrease in the protein expressions of phosphorylated-Rb, cyclin D and Cdk4 and up-regulation of the protein levels of p15INK4B and p27Kip1. Fucoxanthin-induced apoptosis was accompanied with down-regulation of the protein levels of Bcl-xL, and inhibitor of apoptosis protein, resulting in cytochrome c release and sequential activation of caspase-9, caspase-3, and PARP. Furthermore, fucoxanthin activated JNK, MAPK and ERK on B16F10 cells. These results suggest that fucoxanthin has anti-tumor effects on HL-60 and B16F10 cell lines by inducing selectively the genes related to apoptosis which provided further theoretical support for the application of fucoxanthin as a promising anti-tumor agent. which is a scavenger of ROS, suppressed fucoxantin-induced cytotoxicity and apoptosis. Furthermore, the treatment with NAC dramatically inhibited fucoxanthin-induced phosphorylation of JNK and p38 kinase in HL-60 cells. Moreover, fucoxanthin reduced the viability of B16F10 cells in a dose-dependent manner accompanied by the induction of cell cycle arrest during the G0/G1 phase and apoptosis. Fucoxanthin-induced G0/G1 arrest was associated with a marked decrease in the protein expressions of phosphorylated-Rb, cyclin D and Cdk4 and up-regulation of the protein levels of p15INK4B and p27Kip1. Fucoxanthin-induced apoptosis was accompanied with down-regulation of the protein levels of Bcl-xL, and inhibitor of apoptosis protein, resulting in cytochrome c release and sequential activation of caspase-9, caspase-3, and PARP. Furthermore, fucoxanthin activated JNK, MAPK and ERK on B16F10 cells. These results suggest that fucoxanthin has anti-tumor effects on HL-60 and B16F10 cell lines by inducing selectively the genes related to apoptosis which provided further theoretical support for the application of fucoxanthin as a promising anti-tumor agent.
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URI
- https://sciwatch.kiost.ac.kr/handle/2020.kiost/26867
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Bibliographic Citation
- 2013 International Symposium and Annual Meeting of the KSABC, pp.206, 2013
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Publisher
- 한국응용생명화학회
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Type
- Conference
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Language
- English
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