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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/17323


    Title: Inhibition of proliferation of a hepatoma cell line by fucoxanthin in relation to cell cycle arrest and enhanced gap junctional intercellular communication
    Authors: 黃永勝;Huang, Yung-Sheng
    Contributors: 保健營養生技學系
    Keywords: Fucoxanthin;Cytotoxicity;Apoptosis;Connexin 43;Connexin 32;Gap junctional intercellular communication
    Date: 2009
    Issue Date: 2012-11-26 10:31:30 (UTC+8)
    Abstract: Fucoxanthin is one of the most abundant carotenoids found in Undaria pinnatifida and has been shown to inhibit tumor proliferation in vitro. However, the mechanisms underlying the anti-cancer effects of fucoxanthin are unclear. In this study, we hypothesized that fucoxanthin may cause cell cycle arrest and enhance gap junctional intercellular communication (GJIC) in SK-Hep-1 human hepatoma cells. Data revealed that fucoxanthin (1–20 μM) strongly and concentration-dependently inhibited the proliferation of SK-Hep-1 cells at 24 h of incubation, whereas fucoxanthin facilitated the growth of a murine embryonic hepatic (BNL CL.2) cells at 24 h of incubation and only slightly slowed the cell proliferation at 48 h. In SK-Hep-1 cells, fucoxanthin caused cell cycle arrest at G0/G1 phase and induced cell apoptosis, as evidenced by increased subG1 cells and induction of DNA strand breaks. Using scrape loading-dye-transfer assay, fucoxanthin was found to significantly enhance GJIC of SK-Hep-1 cells without affecting that of BNL CL.2 cells. In addition, fucoxanthin significantly increased protein and mRNA expressions of connexin 43 (Cx43) and connexin 32 (Cx32) in SK-Hep-1 cells. Moreover, fucoxanthin markedly increased the concentration of intracellular calcium levels in SK-Hep-1 cells. Thus, fucoxanthin is specifically antiproliferative against SK-Hep-1 cells, and the effect is associated with upregulation of Cx32 and Cx43, which enhances GJIC of SK-Hep-1 cells. The enhanced GJIC may be responsible for the increase of the intracellular calcium level, which then causes cell cycle arrest and apoptosis.
    Relation: CHEMICO-BIOLOGICAL INTERACTIONS; 182(2-3):165-72.
    Appears in Collections:[食品營養與保健生技學系] 期刊論文

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