Effects of Astragaloside on Biological Characteristics of Non-Small Cell Lung Cancer Cells via the Phosphatidylinositol 3-Kinase/Protein Kinase B/Mechanistic Target of Rapamycin Pathway
Citations Over Time
Abstract
To evaluate the effects of astragaloside on the proliferation, invasion, migration and apoptosis of nonsmall cell lung cancer A549 cells and phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of rapamycin pathway. After A549 cells were treated with 0, 10, 20, 40, 60, 80 and 100 μmol/l astragaloside for 24 h, the survival rate was measured by methyl thiazolyl tetrazolium assay and the half maximal inhibitory concentration was calculated. Astragaloside at half maximal inhibitory concentration was added. Cell invasion, migration and apoptosis were detected by transwell assay, wound healing assay and flow cytometry, respectively. The effects of astragaloside on the expressions of phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of rapamycin pathway-related proteins were detected by western blotting. After different concentrations of astragaloside were added, cell proliferation declined with increasing concentration. Half maximal inhibitory concentration against A549 cell proliferation was 32.2 μmol/l. Compared with blank control group; cell proliferation; invasion and migration were significantly weakened, while apoptosis was enhanced in astragaloside group. The expressions of phosphorylation of phosphatidylinositol 3-kinase, phosphorylation of protein kinase B and phosphorylation of mechanistic target of rapamycin proteins in astragaloside group were significantly lower than those in blank control group. Astragaloside inhibits the proliferation, invasion and migration, and promotes the apoptosis of nonsmall cell lung cancer A549 cells dose-dependently. Inhibiting phosphorylation of phosphatidylinositol 3-kinase, phosphorylation of protein kinase B and phosphorylation of mechanistic target of rapamycin expressions in the phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of rapamycin pathway may be one of the mechanisms of astragaloside.
Related Papers
- → FoxO Transcription Factors Promote AKT Ser473 Phosphorylation and Renal Tumor Growth in Response to Pharmacologic Inhibition of the PI3K–AKT Pathway(2014)162 cited
- → Reactivation of AKT signaling following treatment of cancer cells with PI3K inhibitors attenuates their antitumor effects(2013)21 cited
- → Virtual Docking Screening and QSAR Studies to Explore PI3K and mTOR Inhibitors Acting on AKT in Cancers(2020)1 cited
- → Solanine Interferes with AKT/p-AKT and PI3K/p-PI3K Pathway to Inhibit HIF and Destroy Cell Energy Metabolism(2021)1 cited
- → Solanine Interferes With AKT/p-AKT and PI3K/ p-PI3K to Inhibit HIF and Destroy Cell Energy Metabolism(2021)