旨在分析黄芪多糖(astragalus polysaccharides, APS)调控癌胚抗原相关细胞黏附分子7(carcinoembryonic antigen-related cell adhesion molecule 7, CEACAM7)通过上皮-间充质转化(epithelial-mesenchymal transition, EMT)通路，抑制肺癌A549细胞恶性生物学行为的机制。

采用CCK-8法检测APS对A549细胞增殖的影响，流式细胞术检测APS对细胞凋亡的诱导作用，Transwell实验和划痕愈合实验评估APS对细胞侵袭和迁移能力的影响。Western blot检测CEACAM7及EMT相关标志物的表达水平。

CCK-8实验结果显示，与对照组(2.1±0.17)相比，APS处理组100 mg/L、200 mg/L、400 mg/L在第4天OD450值分别为(1.63±0.12)、(1.38±0.11)、(1.09±0.09)，呈现显著剂量依赖性抑制效应(P<0.05)。400 mg/L组细胞增殖抑制率达29.3%，作用24 h后生长曲线偏离对照组趋势。流式细胞术检测结果显示，与对照组相比，APS处理组100 mg/L、200 mg/L、400 mg/L促进A549细胞的凋亡，促凋亡作用呈剂量依赖性，与对照组(16.21±1.32)%相比，100 mg/L、200 mg/L、400 mg/L处理组的凋亡率分别达(26.5±2.32)%、(33.7±3.11)%、(39.4±3.6)%。高剂量组凋亡率较对照组提高(P<0.05)。与对照组的细胞数量(76.32±6.32)个相比，APS处理组100 mg/L、200 mg/L、400 mg/L的细胞数量分别为(57.32±4.16)个、(38.13±2.67)个、(25.30±1.96)个。与对照组的划痕愈合率(69.81±5.16)%相比，APS处理组100 mg/L、200 mg/L、400 mg/L的划痕愈合率分别(57.95±4.66)%、(49.72±4.24)%、(41.56±3.38)%。

APS通过调控CEACAM7通过EMT通路显著抑制了肺癌A549细胞的增殖、侵袭和迁移能力，具有潜在的抗肺癌作用，为开发基于天然药物的肺癌治疗新策略提供了理论依据。

This study aims to investigate the mechanism by which astragalus polysaccharides (APS) regulate carcinoembryonic antigen-related cell adhesion molecule 7 (CEACAM7) and via the epithelial-mesenchymal transition (EMT) pathway to inhibit the malignant biological behavior of lung cancer A549 cells.

The effects of APS on A549 cell proliferation were assessed using the CCK-8 assay. The induction of apoptosis by APS was evaluated using flow cytometry. The impact of APS on cell invasion and migration was assessed using Transwell assays and wound healing assays. Western blot analysis was performed to detect the expression levels of CEACAM7 and EMT-related markers.

The CCK-8 results showed that compared with the control group (2.1±0.17), the OD450 values of 100 mg/L, 200 mg/L and 400 mg/L in the APS treatment group were (1.63±0.12), (1.38±0.11) and (1.09±0.09) respectively on the fourth day. CCK-8 showed that APS inhibited the proliferation and promoted apoptosis of A549 cells in a dose-dependent manner. The high dose group (400 mg/L) showed the most significant inhibition. Flow cytometry showed APS treatment group significantly promoted the apoptosis of A549 cells, and the apoptotic effect was dose-dependent. Compared with the control group, the APS treatment groups (100 mg/L, 200 mg/L, and 400 mg/L) significantly enhanced A549 cell apoptosis with a dose-dependent effect, compared with the control group (16.21±1.32%), the apoptosis rates in 100 mg/L, 200 mg/L and 400 mg/L treatment groups were (26.5±2.32%), (33.7±3.11%) and (39.4±3.6%), respectively. The apoptosis rate in the high dose group was higher than that in the control group (P<0.05). Compared with the cell number of the control group (76.32±6.32), the cell number of APS treatment group at 100 mg/L, 200 mg/L and 400 mg/L was (57.32±4.16), (38.13±2.67) and (25.30±1.96) respectively. Compared with the scratch healing rate of the control group (69.81±5.16)%, the healing rate of 100 mg/L, 200 mg/L and 400 mg/L in APS treatment group was(57.95±4.66)%, (49.72±4.24)% and (41.56±3.38)% respectively.

Astragalus polysaccharides inhibit the proliferation, invasion, and migration of lung cancer A549 cells by regulating CEACAM7 via the EMT pathway. This study provides a theoretical basis for the development of new lung cancer treatment strategies based on natural drugs.