Rapamycin inhibits proliferation and apoptosis of retinoblastoma cells through PI3K/AKT signaling pathway

Effects of Rapamycin on the proliferation and apoptosis of retinoblastoma cells through the phosphatidylinositol 3-hydroxy kinase (PI3K)/protein kinase B (AKT) signaling pathway were studied. The retinoblastoma Y79 cells were selected and divided into negative control group (NC group), 0.2 mu M Rapamycin group and 0.4 mu M Rapamycin group. Then the proliferative activity of Y79 cells was detected using Cell Counting Kit-8 (CCK8) assay, the content of reactive oxygen species (ROS), malondialdehyde (MDA) and superoxide dismutase (SOD) in cells in each group was detected using enzyme-linked immunosorbent assay (ELISA), and the apoptosis of Y79 cells was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. Moreover, the changes in Y79 cell cycle and apoptosis were determined through flow cytometry, and apoptosis and PI3K/AKT pathway were detected using reverse transcription-polymerase chain reaction (RT-PCR) and western blotting. It was found that the number of cells and the proliferative activity were significantly reduced in 0.2 mu M Rapamycin group and 0.4 mu M Rapamycin group. In 0.2 mu M Rapamycin group and 0.4 mu M Rapamycin group, the content of ROS and MDA was significantly decreased, while that of SOD was notably increased. TUNEL assay and flow cytometry showed that in 0.2 mu M Rapamycin group and 0.4 mu M Rapamycin group, the number of apoptotic cells was obviously increased, and the cell cycle was basically arrested in S phase. The expression levels of Bcl-2, PI3K and AKT declined in 0.2 mu M Rapamycin group and 0.4 mu M Rapamycin group, whereas the expression of Caspase 8 increased. Similar results were also obtained in the protein assay. The above results were significantly superior in 0.4 mu M Rapamycin group to those in 0.2 mu M Rapamycin group. Rapamycin inhibits proliferation and promotes apoptosis of retinoblastoma cells through inhibiting the PI3K/AKT signaling pathway.