Salvianolic acid B inhibits the proliferation and metastasis of A549 lung cancer cells via miR-23a/PTEN/AKT pathway.

Salvianolic acid B (Sal B), a polyphenolic compound with potential anti-cancer properties, possesses mechanisms of action that remain incompletely understood. This study aimed to elucidate the effects of Sal B on the A549 cell line and to investigate the underlying molecular mechanisms. In this study, A549 cells were co-cultured with varying concentrations of Sal B for 48 h. We utilized MTT, wound healing, and transwell assays to evaluate cell proliferation, migration, and invasion, respectively. The expression levels of miR-23a-3p, E-cadherin, N-cadherin, Snail, PTEN, and p-AKT were analyzed using western blotting and RT-PCR. Additionally, a xenograft model of transplanted A549 tumors was employed to assess the in vivo antitumor effects of Sal B. Immunohistochemistry (IHC) was utilized to measure the expression of cleaved PARP, E-cadherin, N-cadherin and Snail. Our findings demonstrated that Sal B inhibited A549 cell proliferation, migration, and invasion in a dose-dependent manner. Furthermore, in vivo experiments revealed that Sal B significantly suppressed the growth and metastasis of A549 tumors, as evidenced by elevated levels of cleaved PARP and E-cadherin, along with a marked reduction in N-cadherin and Snail compared with the control group. Importantly, we observed that Sal B significantly downregulated miR-23a-3p expression, whereas the overexpression of miR-23a-3p via transfection attenuated the inhibitory effects of Sal B on A549 cell proliferation and metastasis. Western blot results indicated that the downregulation of miR-23a-3p led to the upregulation of PTEN and the downregulation of p-AKT. Collectively, these findings suggest that Sal B's mechanism of action in NSCLC may involve the modulation of the miR-23a/PTEN/AKT signaling pathway, thereby highlighting its potential as a therapeutic candidate for NSCLC.