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논문 기본 정보

자료유형
학술저널
저자정보
Ji, Yu-Bin (Engineering Research Center of Natural Anticancer Drugs, Harbin University of Commerce) Chen, Ning (Engineering Research Center of Natural Anticancer Drugs, Harbin University of Commerce) Zhu, Hong-Wei (State Key Laboratory for Molecular Biology of Special Economic Animals, Institute of Special Animal and Plant Sciences, Chinese Academy of Agricultural Sciences) Ling, Na (Engineering Research Center of Natural Anticancer Drugs, Harbin University of Commerce) Li, Wen-Lan (Engineering Research Center of Natural Anticancer Drugs, Harbin University of Commerce) Song, Dong-Xue (Engineering Research Center of Natural Anticancer Drugs, Harbin University of Commerce) Gao, Shi-Yong (Engineering Research Center of Natural Anticancer Drugs, Harbin University of Commerce) Zhang, Wang-Cheng (Engineering Research Center of Natural Anticancer Drugs, Harbin University of Commerce) Ma, Nan-Nan (Engineering Research Center of Natural Anticancer Drugs, Harbin University of Commerce)
저널정보
아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제15권 제21호
발행연도
2014.1
수록면
9,319 - 9,325 (7page)

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Alkaloids are the most extensively featured compounds of natural anti-tumor herbs, which have attracted much attention in pharmaceutical research. In our previous studies, a mixture of major three alkaloid components (5, 6-dihydrobicolorine, 7-deoxy-trans-dihydronarciclasine, littoraline) from Hymenocallis littoralis were extracted, analyzed and designated as AHL. In this paper, AHL extracts were added to human liver hepatocellular cells HepG-2, human gastric cancer cell SGC-7901, human breast adenocarcinoma cell MCF-7 and human umbilical vein endothelial cell EVC-304, to screen one or more AHL-sensitive tumor cell. Among these cells, HepG-2 was the most sensitive to AHL treatment, a very low dose ($0.8{\mu}g/ml$) significantly inhibiting proliferation. The non-tumor cell EVC-304, however, was not apparently affected. Effect of AHL on HepG-2 cells was then explored. We found that the AHL could cause HepG-2 cycle arrest at G2/M checkpoint, induce apoptosis, and interrupt polymerization of microtubules. In addition, expression of two cell cycle-regulated proteins, CyclinB1 and CDK1, was up-regulated upon AHL treatment. Up-regulation of the Fas, Fas ligand, Caspase-8 and Caspase-3 was observed as well, which might imply roles for the Fas/FsaL signaling pathway in the AHL-induced apoptosis of HepG-2 cells.

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