Induction of apoptosis by Polygonatum odoratum lectin and its molecular mechanisms in murine fibrosarcoma L929 cells

• Published in: Biochimica et biophysica acta Vol. 1790; no. 8; pp. 840 - 844
• Main Authors: Liu, Bo, Zhang, Bo, Min, Ming-wei, Bian, He-jiao, Chen, Long-fei, Liu, Qian, Bao, Jin-ku
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.08.2009
• Subjects: Animals; Apoptosis; Apoptosis - drug effects; Caspases - metabolism; Cell Line, Tumor; Death-receptor; Drug Screening Assays, Antitumor; Fibrosarcoma - enzymology; Fibrosarcoma - pathology; Mice; Mitochondria; Mitochondria - drug effects; Mitochondria - metabolism; Phytotherapy; Plant Lectins - pharmacology; Polygonatum - metabolism; Polygonatum odoratum Lectin (POL); Receptors, Death Domain - metabolism; The Galanthus nivalis agglutinin (GNA)-related lectins; Tumor necrosis factor α (TNFα); Tumor Necrosis Factor-alpha - pharmacology; Polygonatum odoratum Lectin (POL); Mitochondria; The Galanthus nivalis agglutinin (GNA)-related lectins; Tumor necrosis factor α (TNFα); Death-receptor; Apoptosis
• ISSN: 0304-4165; 0006-3002; 1872-8006
• DOI: 10.1016/j.bbagen.2009.04.020

The Galanthus nivalis agglutinin (GNA)-related lectins have been reported to bear antiproliferative and apoptosis-inducing activities in cancer cells; however, the precise mechanisms by which GNA-related lectins induce cell death are still only rudimentarily understood. In the present study, Polygonatum odoratum lectin (designated POL), a mannose-binding specific GNA-related lectin, possessed a remarkable antiproliferative activity toward murine fibrosarcoma L929 cells. And, this lectin induced L929 cell apoptosis in a caspase-dependent manner. In addition, POL treatment increased the levels of FasL and Fas-Associated protein with Death Domain (FADD) proteins and resulted in caspase-8 activation. Also, POL treatment caused mitochondrial transmembrane potential collapse and cytochrome c release, leading to activations of caspase-9 and caspase-3. Moreover, POL treatment enhanced tumor necrosis factor α (TNFα)-induced L929 cell apoptosis. Our data demonstrate for the first time that this lectin induces apoptosis through both death-receptor and mitochondrial pathways, as well as amplifies TNFα-induced L929 cell apoptosis. These inspiring findings would provide new molecular basis for further understanding cell death mechanisms of the Galanthus nivalis agglutinin (GNA)-related lectins in future cancer investigations.