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Lung cancer (LC) is the highest lethality in all tumors. Non-small cell lung cancer (NSCLC) accounts for about 80% of all LC. Acanthopanax senticosus polysaccharide (ASPS) is extracted from the root of Acanthopanax senticosus (AS). Herein, we examined the effect and molecular mechanism of ASPS on NSCLC. The proliferation, invasion and migration of NCI-H520 cells were detected by cell counting kit-8 (CCK-8), transwell assay and wound healing assay, respectively. The epithelial-mesenchymal transition (EMT) and Wnt/β-catenin pathway-related factors were evaluated using quantitative real-time PCR (QRT-PCR) and western blot assay. Our results observed that ASPS significantly decreased the proliferation of cells at 24 and 48 h. Moreover, ASPS markedly repressed the invasion and migration capacities of cells in a concentration-dependent manner. Besides, ASPS obviously down-regulated the levels of matrix metalloproteinase-2 (MMP-2), MMP-9, fibronectin 1 (FN1), vimentin, wnt3a, phosphorylated-glycogen synthase kinase 3β (p-GSK3β) and cyclin D1, whereas, up-regulating E-cadherin level. The level of GSK3β was not changed in the different groups. ASPS conspicuously inhibited the abilities of proliferation and metastasis in human non-small cell lung cancer cell line NCI-H520 possibly by suppressing Wnt/β-catenin pathway mediated-EMT.

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Acanthopanax senticosus polysaccharide suppressing proliferation and metastasis of the human non-small cell lung cancer NCI-H520 cells is associated with Wnt/β-catenin signaling