Fucoxanthin suppresses tumor growth of human leukemia HL-60 cells and melanoma B16F10 cells in vitro and in vivo
DC Field | Value | Language |
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dc.contributor.author | 김민선 | - |
dc.contributor.author | 장지이 | - |
dc.contributor.author | 예보람 | - |
dc.contributor.author | 이아름 | - |
dc.contributor.author | 김길남 | - |
dc.contributor.author | 이승홍 | - |
dc.contributor.author | 고석천 | - |
dc.contributor.author | 정원교 | - |
dc.contributor.author | 허수진 | - |
dc.date.accessioned | 2020-07-16T03:52:16Z | - |
dc.date.available | 2020-07-16T03:52:16Z | - |
dc.date.created | 2020-02-11 | - |
dc.date.issued | 2014-08-25 | - |
dc.identifier.uri | https://sciwatch.kiost.ac.kr/handle/2020.kiost/26050 | - |
dc.description.abstract | The purpose of 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. This study suggested 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.lls, 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. This study suggested 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. | - |
dc.description.uri | 2 | - |
dc.language | English | - |
dc.publisher | Korean | - |
dc.relation.isPartOf | Creative Food Science for the Future | - |
dc.title | Fucoxanthin suppresses tumor growth of human leukemia HL-60 cells and melanoma B16F10 cells in vitro and in vivo | - |
dc.type | Conference | - |
dc.citation.conferencePlace | KO | - |
dc.citation.endPage | 126 | - |
dc.citation.startPage | 126 | - |
dc.citation.title | Creative Food Science for the Future | - |
dc.contributor.alternativeName | 김민선 | - |
dc.contributor.alternativeName | 장지이 | - |
dc.contributor.alternativeName | 예보람 | - |
dc.contributor.alternativeName | 이아름 | - |
dc.contributor.alternativeName | 허수진 | - |
dc.identifier.bibliographicCitation | Creative Food Science for the Future, pp.126 | - |
dc.description.journalClass | 2 | - |