12--Napelline Inhibits Leukemia Cell Proliferation via the PI3K/AKT Signaling Pathway and .

This study aimed to investigate the inhibitory effect of 12--napelline on leukemia cells and its possible mechanisms. The inhibitory effects of 12--napelline on K-562 and HL-60 cells were evaluated using the CCK-8 assay, cell cycle arrest and apoptosis were detected by flow cytometry, and the expression of related proteins was measured by western blot. A K-562 tumor model was established to evaluate the antitumor effect of 12--napelline . A reduction in leukemia cell viability was observed after treatment with 12--napelline. It was determined that the cell cycle was arrested in the 0/1 phase, and the cell apoptosis rate was increased. Moreover, caspase-3 and Bcl-2 were downregulated, whereas cleaved caspase-3 and caspase-9 were upregulated. Further study revealed that 12--napelline could suppress the expression of PI3K, AKT, p-AKT, and mTOR. Insulin-like growth factor 1 (IGF-1) attenuated 12--napelline-induced apoptosis and ameliorated the repression of PI3K, AKT, p-AKT, and mTOR by 12--napelline. Animal experiments clearly showed that 12--napelline inhibited tumor growth. In conclusion, 12--napelline restrained leukemia cell proliferation by suppressing the PI3K/AKT/mTOR pathway and