Rapamycin inhibits proliferation and apoptosis of retinoblastoma cells through PI3K/AKT signaling pathway
Authors:
Open Access
- 30 January 2020
- journal article
- research article
- Published by Spandidos Publications in Oncology Letters
- Vol. 19 (4) , 2950-2956
Abstract
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 µM Rapamycin group and 0.4 µM 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 µM Rapamycin group and 0.4 µM Rapamycin group. In 0.2 µM Rapamycin group and 0.4 µM 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 µM Rapamycin group and 0.4 µM 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 µM Rapamycin group and 0.4 µM 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 µM Rapamycin group to those in 0.2 µM Rapamycin group. Rapamycin inhibits proliferation and promotes apoptosis of retinoblastoma cells through inhibiting the PI3K/AKT signaling pathway.Keywords
This publication has 23 references indexed in Scilit:
- Methyl eugenol induces potent anticancer effects in RB355 human retinoblastoma cells by inducing autophagy, cell cycle arrest and inhibition of PI3K/mTOR/Akt signalling pathway2018
- Correlations between claudin-1 and PIGF expressions in retinoblastoma2018
- LncRNA MT1JP acts as a tumor inhibitor via reciprocally regulating Wnt/β-Catenin pathway in retinoblastoma2018
- Essential oil ofCephalotaxus griffithiineedle inhibits proliferation and migration of human cervical cancer cells: involvement of mitochondria-initiated and death receptor-mediated apoptosis pathwaysNatural Product Research, 2014
- Isoegomaketone induces apoptosis in SK-MEL-2 human melanoma cells through mitochondrial apoptotic pathway via activating the PI3K/Akt pathwayInternational Journal of Oncology, 2014
- Activation of the PI3K/mTOR/AKT Pathway and Survival in Solid Tumors: Systematic Review and Meta-AnalysisPLOS ONE, 2014
- Antiproliferative and Apoptotic Effects of Indomethacin on Human Retinoblastoma Cell Line Y79 and the Involvement of ß-Catenin, Nuclear Factor-κB and Akt Signaling PathwaysOphthalmic Research, 2013
- Rapamycin Inhibits the Production of Myofibroblasts and Reduces Corneal Scarring After Photorefractive KeratectomyInvestigative Ophthalmology & Visual Science, 2013
- Survival with retinoblastoma in the USA: 1975-2004British Journal of Ophthalmology, 2008
- Rapamycin (AY-22,989), a new antifungal antibiotic. I. Taxonomy of the producing streptomycete and isolation of the active principle.The Journal of Antibiotics, 1975