A novel synthetic chitosan selenate (CS) induces apoptosis in A549 lung cancer cells via the Fas/FasL pathway.

Selenium is important to human health, particularly for immune response and cancer prevention. Chitosan has good biocompatibility and low toxicity. In this paper, we synthesized chitosan selenate (CS), a novel therapeutic compound, using chitosan and selenium. CS synthesis was evaluated using FTIR, which verified the presence of a characteristic SeO absorption peak at 892 cm, and with HPGPC, which calculated the molecular weight as approximately 41.8 kDa. Next, we evaluated the proliferation-inhibitory and apoptosis-inducing effects of CS on lung cancer A549 cells and explored its potential molecular mechanisms. MTT assay indicated that CS could significantly inhibit A549 cells viability in a dose-dependent manner. Typical morphological features of apoptosis were observed by Hoechst staining in A549 cells treated with CS, and Annexin V-FITC/PI staining confirmed that CS induced cell death via apoptosis and not necrosis. Cell cycle detection showed that CS triggered S and G2/M phase arrest in a dose-dependent manner. Finally, western blot analysis indicated that CS up-regulated the expression levels of Fas, FasL, and Fadd; subsequently, activated the caspase cascade in A549 cells. These results show that CS induces apoptosis in A549 cells via the Fas/FasL signaling pathway, and has potential chemopreventive effects for lung cancer treatment.