Polygonatum cyrtonema lectin induces murine fibrosarcoma L929 cell apoptosis and autophagy via blocking Ras–Raf and PI3K–Akt signaling pathways

• DOI: 10.1016/j.biochi.2010.08.009
• Publication Date: 2010-08-15T04:36:41Z
• Authors: Bo Liu; Jin-ming Wu; Jing Li; Jun-jie Liu; Wen-wen Li; Chun-yang Li; Huai-long Xu; Jin-ku Bao
• Keywords: 0301 basic medicine; Indoles; Dose-Response Relationship, Drug; Cell Survival; Fibrosarcoma; Blotting, Western; Polygonatum; Apoptosis; Polyenes; Heterocyclic Compounds, 4 or More Rings; 3. Good health; Androstadienes; Mice; Phosphatidylinositol 3-Kinases; 03 medical and health sciences; Microscopy, Electron, Transmission; Phenols; Cell Line, Tumor; Autophagy; Animals; Plant Lectins; Cell Proliferation; Phosphoinositide-3 Kinase Inhibitors

Polygonatum cyrtonema lectin (PCL), a mannose/sialic acid-binding lectin, has been reported to display remarkable anti-proliferative and apoptosis-inducing activities toward a variety of cancer cells; however, the precise molecular mechanisms by which PCL induces cancer cell death are still elusive. In the current study, we found that PCL could induce apoptosis and autophagy in murine fibrosarcoma L929 cells. Subsequently, we demonstrated that inhibition of Ras could promote L929 cell death, suggesting that Ras-Raf signaling pathway plays the key negative regulator in PCL-induced apoptosis. And, we showed that Ras-Raf signaling pathway was also involved in PCL-induced autophagy as the negative regulator. In addition, we found that class I phosphatidylinositol 3-kinase (PI3K)-Akt signaling pathway could play the negative regulator in PCL-induced apoptosis and autophagy. Taken together, these results demonstrate that PCL induces murine fibrosarcoma L929 cell apoptosis and autophagy via blocking Ras-Raf and PI3K-Akt signaling pathways.