Objective. To study the effect of Codonopsis pilosula polysaccharide (CPP) on the growth and motility of HepG2 cells and its possible mechanism. Methods. Cells were randomly divided into Control group, CPP (5 μM) group, CPP (10 μM) group, and CPP (20 μM) group. The proliferation, invasion, migration ability, and expression of proteins involved in the epithelial-mesenchymal transition (EMT) and signaling pathway of HepG2 cells were detected by CCK8 assay, BrdU staining, Transwell, Scratch test, and Western blot, respectively. Results. Codonopsis pilosula polysaccharide inhibited the proliferation of HepG2 cells cultured in vitro along with the expression level of Ki67 and PCNA protein (), decreased the number of invasive cells (), and reduced the scratch closure rate (). It also adjusted the expression of vascular endothelial growth factor (VEGF), E-cadherin, and N-cadherin (). Other than that, downregulation of β-catenin, TCF4, and c-Myc protein expression () was observed as well. Conclusion. Codonopsis pilosula polysaccharide can inhibit the proliferation and motility of HepG2 cells cultured in vitro, and the underlying mechanism is proposed to be related to the inhibition of the β-catenin/TCF4 pathway.

中文翻译：

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党参多糖通过调节β-Catenin/ TCF4途径对肝癌细胞HepG2细胞生长和运动的影响

目标。研究党参党参多糖（CPP）对HepG2细胞生长和运动的影响及其可能的机制。方法。细胞随机分为对照组，CPP（5  μ M）基团，CPP（10  μ M）基团，和CPP（20  μ M）基团。通过CCK8检测，BrdU染色，Transwell，Scratch试验和Western blot分别检测HepG2细胞的上皮-间质转化（EMT）和信号通路的蛋白的增殖，侵袭，迁移能力和蛋白表达。结果。党参多糖抑制体外培养的HepG2细胞增殖以及Ki67和PC​​NA蛋白的表达水平（），减少了侵袭性细胞的数量（），并降低了划痕闭合率（）。它还调节了血管内皮生长因子（VEGF），E-钙黏着蛋白和N-钙黏着蛋白的表达（）。除此之外， β -catenin，TCF4和c-Myc蛋白表达下调（）也被观察到。结论。党参党参多糖可以抑制体外培养的HepG2细胞的增殖和运动，其潜在机制被认为与抑制β -catenin/ TCF4途径有关。