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Alkaloids from Beach Spider Lily (Hymenocallis littoralis) Induce Apoptosis of HepG-2 Cells by the Fas-signaling Pathway

  • 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)
  • Published : 2014.11.28

Abstract

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.

Acknowledgement

Supported by : Chinese Ministry of Education, Natural Science Foundation of Heilongjiang Province

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