Lepista sordida polysaccharide induces apoptosis of Hep-2 cancer cells via mitochondrial pathway

• Published in: International journal of biological macromolecules 2013-10, Vol.61, p.97-101
• Main Authors: Miao, Susheng, Mao, Xionghui, Pei, Rong, Miao, Suping, Xiang, Cheng, Lv, Yuanjing, Yang, Xianguang, Sun, Ji, Jia, Shenshan, Liu, Yvpeng
• Format: Article
• Language: English
• Subjects: antineoplastic agents; Apoptosis; Apoptosis - drug effects; Basidiomycota - chemistry; caspase-3; Caspases - metabolism; Cell Cycle Checkpoints - drug effects; cell proliferation; Cell Survival - drug effects; cytochrome c; Cytochromes c - metabolism; Dose-Response Relationship, Drug; Enzyme Activation - drug effects; fruiting bodies; Fungal Polysaccharides - chemistry; Fungal Polysaccharides - pharmacology; Hep G2 Cells; human cell lines; Humans; Laryngocarcinoma; Lepista; Lepista sordida; membrane potential; Membrane Potential, Mitochondrial - drug effects; Mitochondria - drug effects; Mitochondria - metabolism; mitochondrial membrane; Mitochondrial pathway; neoplasm cells; Polysaccharide; polysaccharides; Proto-Oncogene Proteins c-bcl-2 - metabolism; Signal Transduction - drug effects
• ISSN: 0141-8130; 1879-0003
• DOI: 10.1016/j.ijbiomac.2013.06.052

In our previous study, a potential antitumor polysaccharide (LSPc1) was screened from the fruiting bodies of Lepista sordida. However, its molecular mechanism of cell death induction on Hep-2 human laryngocarcinoma cells has still not been determined. The present study evaluated the anticancer efficacy and associated mechanisms of LSPc1 on Hep-2 cells in vitro. We found that LSPc1-induced inhibition of cell proliferation was associated with an increase in G2/M-phase arrest at 48h. Typical morphological and biochemical features of apoptosis were also observed in LSPc1-treated cells. Furthermore, LSPc1 led a loss of mitochondrial membrane potential (ΔΨm), increased the ratio of pro-apoptotic Bax to anti-apoptotic Bcl-2, induced cytochrome c release, and increased the activity of caspase-3 and -9, which altogether account for apoptotic cell death. Taken together, our study suggests that intrinsic mitochondrial caspase dependent pathway plays a very important role in LSPc1-induced cancer apoptosis and these results provided strong experimental evidence for the use of LSPc1 as a potential therapeutic agent in cancer for laryngocarcinoma.