Astragalus Polysaccharides Inhibit Pancreatic Cancer Progression by Downregulation of TLR4/NF-κB Signaling Pathway

Background. Pancreatic cancer (PC) leads to high human malignancy mortality worldwide. This study explored the role of Astragalus polysaccharide (APS) on human PC PANC-1 cells and its underlying mechanisms. Method. Cell viability, proliferation, apoptosis, invasion, and migration were measured by CCK-8, EdU incorporation, flow cytometry, Transwell, and wound healing assay, respectively. ELISA assay was utilized to detect the IL-1 alpha, IL-4, IL-6, IL-8, and TNF-alpha levels. The western blot assay was performed to measure the level changes of cell function-related proteins. The transportation of NF-kappa B P65 protein was detected through immunofluorescence assay. Results. Compared with the control group, APS treatment could significantly inhibit cell proliferation. APS treatment could also suppress cell migration and invasion ability and induce apoptosis and inflammation in PANC-1 cells. Furthermore, APS inhibited the activation of TLR4/NF-kappa B signaling pathway via suppressing the phosphorylation and transportation of NF-kappa B P65 into the PANC-1 cell nucleus. Conclusion. APS suppresses PANC-1 cell viability, proliferation, migration, and invasion while inducing inflammation and apoptosis. APS might regulate PC cell motility via downregulating TLR4/NF-kappa B signaling pathway.