SOS1-IT1 silencing alleviates MPP+-induced neuronal cell injury through regulating the miR-124-3p/PTEN/AKT/mTOR pathway.

Long non-coding RNA (lncRNA) has been found to be involved in the regulation of a variety of disease progression, including Parkinson's disease (PD). However, the role and underlying mechanism of SOS1 intronic transcript 1 (SOS1-IT1) in the progression of PD is still unclear. 1-methyl-4-phenyl pyridine (MPP+) induced SK-N-SH cells were used to construct PD cell models in vitro. The expression levels of SOS1-IT1, microRNA (miR)-124-3p and phosphatase and tensin homolog (PTEN) were determined using quantitative real-time PCR. Cell counting kit 8 assay and flow cytometry were used to measure cell viability and apoptosis. Western blot analysis was performed to detect protein expression. The levels of inflammation cytokines and oxidative stress markers were examined to assess cell inflammation and oxidative stress. In addition, dual-luciferase reporter assay, RIP assay and RNA pull-down assay were used to confirm RNA interaction. Our results showed that SOS1-IT1 was upregulated in MPP+-induced SK-N-SH cells, and its silencing reversed the inhibition effect of MPP+ on the viability and the promotion effect on the apoptosis, inflammation and oxidative stress of SK-N-SH cells. MiR-124-3p was targeted by SOS1-IT1, and its inhibitor reversed the suppressive effect of SOS1-IT1 knockdown on MPP+-induced SK-N-SH cell injury. Furthermore, PTEN was a target of miR-124-3p, and the reduction effect of miR-124-3p on MPP+-induced SK-N-SH cell injury was reversed by PTEN overexpression. Additionally, the activity of AKT/mTOR pathway was regulated by the SOS1-IT1/miR-124-3p/PTEN axis. In conclusion, SOS1-IT1 regulated the miR-124-3p/PTEN/AKT/mTOR pathway to participate in the regulation of MPP+-induced neuronal cell injury, indicating the SOS1-IT1 might be an effective therapeutic target for PD.