Dehydrocavidine inhibits proliferation and induces apoptosis in human lung adenocarcinoma A549 cells

To investigate the effects of dehydrocavidine on the proliferation and apoptosis of human lung adenocarcinoma A549 cells and to explore its potential mechanisms of action. Human lung adenocarcinoma A549 cells in the logarithmic growth phase were treated with various concentrations of dehydrocavidine. The CCK-8 assay was used to assess cell proliferation. Flow cytometry was employed to evaluate apoptosis and cell cycle distribution. A nude mouse xenograft model of lung adenocarcinoma was established using A549 cells. The mice were randomly divided into a negative control group and two dehydrocavidine treatment groups (high-dose and low-dose). Cisplatin was used as positive control drug. Tumor growth curves were generated based on changes in tumor volume, and tumor inhibition rates were calculated based on final tumor weights. Hematoxylin-eosin (HE) staining was used to observe morphological changes in tumor tissues. Immunohistochemistry was used to detect the expression of cleaved caspase-3 and survivin in xenograft tissues. Dehydrocavidine arrested the cell cycle at the G0/G1 phase and inhibited the proliferation of A549 cells. The IC50 at 24 h, 48 h, and 72 h were 118.7µM, 15.06 µM, and 14.36 µM, respectively. Dehydrocavidine effectively promoted apoptosis in A549 cells in a dose-dependent manner. In the xenograft model, Dehydrocavidine significantly inhibited tumor growth. The tumor weight inhibition rates in the high- and low-dose groups were 32.34% and 20.18%, respectively. Compared with the negative group, the expression levels of cleaved caspase-3 and survivin in tumor tissues were significantly altered in all treatment groups ( P < 0.05). Dehydrocavidine inhibits proliferation and promotes apoptosis of A549 cells both in vitro and in vivo. Its mechanism may involve downregulation of survivin expression and upregulation of cleaved caspase-3, thereby suppressing tumor cell proliferation and inducing apoptosis.