Shikonin promotes apoptosis of non-small cell lung cancer cells and its mechanisms associated with phosphatidylinositol-3-kinase/protein kinase b/mammalian rapamycin target protein signaling pathway

Abstract

Objective To explore the mechanism of shikonin promoting apoptosis of non-small cell lung cancer cells and its association with phosphatidylinositol-3-kinase/protein kinase B/mammalian rapamycin target protein (PI3K/Akt/mTOR) signaling pathway. Methods Non-small cell lung cancer A549 cells were divided into blank group, low, medium and high concentration group. The blank group was cultured with PBS solution and sterile saline. The low concentration group, middle concentration group and high concentration group were cultured with shikonin at different concentrations. Tetrazolium salt (MTT) and flow cytometry were used to detect the proliferation and apoptosis of breast cancer cells at different time points. Western blotting was used to detect the relative expression of PI3K/Akt/mTOR signaling pathway protein. Results At different time points, the proliferation rates of non-small cell lung cancer A549 in low concentration group, medium concentration group and high concentration group were significantly lower than those in high concentration group. The proliferation rate of non-small cell lung cancer A549 in high concentration group was significantly lower than that in low concentration group and medium concentration group at different time points (F=2.622, 3.785, 3.357, P<0.05). At different time points, the apoptotic rate of non-small cell lung cancer A549 in low concentration group, medium concentration group and high concentration group were significantly higher. In the blank group, the apoptotic rate of non-small cell lung cancer A549 in the high concentration group was significantly higher than that in the low concentration group and the medium concentration group at different time points (F=18.103, 28.591, 24.052, P<0.05). The relative expression levels of PI3K, Akt and mTOR protein in low concentration group, medium concentration group and high concentration group were lower than those in blank group, while the relative expression levels of PI3K, Akt and mTOR protein in high concentration group (0.45±0.01, 0.50±0.01, 0.48±0.05) were lower than those in low concentration group (0.98±0.13, 0.86±0.15, 1.00±0.15); The difference was statistically significant in the medium concentration group (0.71±0.09, 0.62±0.08, 0.76±0.10) (F=4.158, 0.072, 2.919, 7.520, 2.633, 18.875, P<0.05). Western blotting results of PI3K/Akt/mTOR signaling pathway-related proteins were consistent with those of the above signaling pathway-related proteins. Conclusion Shikonin can promote apoptosis of non-small cell lung cancer cells. Its mechanism may be related to PI3K/Akt/mTOR signaling pathway, regulating pathway-related proteins and promoting apoptosis of non-small cell lung cancer cells. Key words: Shikonin; Non-small cell lung cancer; Apoptosis