Polygonatum cyrtonema lectin, a potential antineoplastic drug targeting programmed cell death pathways

• Published in: Biochemical and biophysical research communications 2011-03, Vol.406 (4), p.497-500
• Main Authors: Wang, Shu-ya, Yu, Qi-jia, Bao, Jin-ku, Liu, Bo
• Format: Article
• Language: English
• Subjects: Amino Acid Sequence; Antineoplastic Agents - chemistry; Antineoplastic Agents - pharmacology; Apoptosis; Autophagy; Autophagy - drug effects; Caspases - metabolism; Cell Line, Tumor; Humans; Molecular Sequence Data; Phosphatidylinositol 3-Kinases - metabolism; Plant lectin; Plant Lectins - chemistry; Plant Lectins - pharmacology; Polygonatum - chemistry; Polygonatum cyrtonema lectin (PCL); Programmed cell death (PCD); Protein Conformation; Proto-Oncogene Proteins c-akt - metabolism; raf Kinases - metabolism; ras Proteins - metabolism; Reactive Oxygen Species - metabolism
• ISSN: 0006-291X; 1090-2104
• DOI: 10.1016/j.bbrc.2011.02.049

► Polygonatum cyrtonema lectin (PCL) bears remarkable anti-tumor activities toward various cancer cells. ► PCL induces cancer cell apoptotic death via the caspase-dependent pathway, mitochondria-mediated ROS–p38–p53 pathway, Ras–Raf and PI3K–Akt pathways. ► PCL induces cancer cell autophagic death via activating mitochondrial ROS–p38–p53 pathway, as well as via blocking Ras–Raf and PI3K–Akt pathways. ► Polygonatum cyrtonema lectin (PCL) would be utilized as a potential anti-tumor drug targeting programmed cell death pathways. Polygonatum cyrtonema lectin (PCL), a mannose/sialic acid-binding plant lectin, has recently drawn a rising attention for cancer biologists because PCL bears remarkable anti-tumor activities and thus inducing programmed cell death (PCD) including apoptosis and autophagy in cancer cells. In this review, we focus on exploring the precise molecular mechanisms by which PCL induces cancer cell apoptotic death such as the caspase-dependent pathway, mitochondria-mediated ROS–p38–p53 pathway, Ras–Raf and PI3K–Akt pathways. In addition, we further elucidate that PCL induces cancer cell autophagic death via activating mitochondrial ROS–p38–p53 pathway, as well as via blocking Ras–Raf and PI3K–Akt pathways, suggesting an intricate relationship between autophagic and apoptotic death in PCL-induced cancer cells. In conclusion, these findings may provide a new perspective of Polygonatum cyrtonema lectin (PCL) as a potential anti-tumor drug targeting PCD pathways for future cancer therapeutics.