Inhibition of tumor growth in vitro and in vivo by fucoxanthin against human leukemia HL-60 cells and melanoma B16F10 cells

Title
Inhibition of tumor growth in vitro and in vivo by fucoxanthin against human leukemia HL-60 cells and melanoma B16F10 cells
Author(s)
허수진; 예보람; 장지이; 김준성; 김민선; 김지형; 이영득; 이수진; 오철홍; 강도형
KIOST Author(s)
Heo, Soo Jin(허수진)Kim, Junseong(김준성)Lee, Youngdeuk(이영득)Oh, Chulhong(오철홍)Kang, Do-Hyung(강도형)
Publication Year
2013-07-10
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.
URI
https://sciwatch.kiost.ac.kr/handle/2020.kiost/26867
Bibliographic Citation
2013 International Symposium and Annual Meeting of the KSABC, pp.206, 2013
Publisher
한국응용생명화학회
Type
Conference
Language
English
Publisher
한국응용생명화학회
Related Researcher
Research Interests

Marine Life Science,Marine Natural Products,Bioactivities,해양생명과학,해양천연물학,생리활성

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