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|標題:||Inhibition of proliferation of a hepatoma cell line by fucoxanthin in relation to cell cycle arrest and enhanced gap junctional intercellular communication||作者:||Liu, C.L.
|關鍵字:||Fucoxanthin;Cytotoxicity;Apoptosis;Connexin 43;Connexin 32;Gap;junctional intercellular communication;cancer cells;carotenoids;apoptosis;progression;growth;assay;connexin-43;expression;survival;channels||Project:||Chemico-Biological Interactions||期刊/報告no：:||Chemico-Biological Interactions, Volume 182, Issue 2-3, Page(s) 165-172.||摘要:||
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 mu M) 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 CL2) 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 CL2 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. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
|Appears in Collections:||食品暨應用生物科技學系|
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