The aim of this study is to examine the suppressive impact of astragaloside on the invasion and spread of non-small cell lung cancer by obstructing the transforming growth factor-beta/focal adhesion kinase/protein kinase B signaling pathway. Sixty mice were categorized into three groups; the normal control group (n=20) (group A), the model control group (n=20) (group B), and the astragaloside IV intervention group (n=20) (group C). To establish the non-small cell lung cancer mouse model for group B and group C, the modulated PC9/ER cell suspension was injected into the left axilla of nude mice, whereas group A received an equivalent amount of normal saline instead. After successful modeling, mice in group C were given astragaloside 30 mg/kg by intragastric administration. The expression levels of transforming growth factor-beta, focal adhesion kinase, and protein kinase B messenger ribonucleic acid were higher in group B compared to group A, whereas the expression levels of transforming growth factor-beta, focal adhesion kinase, and protein kinase B messenger ribonucleic acid were lower in group C compared to group B. The levels of protein expression for transforming growth factor-beta, focal adhesion kinase, and protein kinase B were higher in group B compared to group A, whereas the levels of protein expression for transforming growth factor-beta, focal adhesion kinase, and protein kinase B were lower in group C compared to group B. The non-small cell lung cancer is influenced by astragaloside A, transforming growth factor-beta, focal adhesion kinase, and protein kinase B.