Overexpression of lncRNA ANRIL aggravated hydrogen peroxide-disposed injury in PC-12 cells via inhibiting miR-499a/PDCD4 axis-mediated PI3K/Akt/mTOR/p70S6K pathway.

Spinal cord injury (SCI) is a grievous neurology-related disorder that causes many devastating symptoms. This research planned to dig the function and latent mechanisms of long noncoding RNA (lncRNA) ANRIL on hydrogen peroxide (H2O2)-disposed injury in PC-12 cells. The PC-12 cells were disposed with H2O2 for 24 h to construct the SCI model. H2O2-disposed PC-12 cells was assessed by detecting cell viability, migration, invasion, apoptosis and autophagy. The level of ANRIL in H2O2-disposed PC-12 cells was analysed, afterwards, the impacts of ANRIL silencing on H2O2-disposed PC-12 cell injury was determined. The regulatory association between ANRIL and miR-499a, between miR-499a and PDCD4, as well as PDCD4 and PI3K/Akt/mTOR/p70S6K signals were investigated. H2O2 produced PC-12 cell injury and promoted the level of ANRIL. Silencing of ANRIL inhibited H2O2-disposed PC-12 cell injury through promoting cell viability, migration, invasion and inhibiting apoptosis and autophagy. Moreover, miR-499a was upregulated after silencing of ANRIL, and inhibition of miR-499a reversed the effects of silencing of ANRIL on H2O2-disposed PC-12 cell injury. Also, PDCD4 was a target of miR-499a. Furthermore, ANRIL silencing alleviated the H2O2-disposed injury in PC-12 cells possible by activating PI3K/Akt/mTOR/p70S6K signals, which was mediated by miR-499a/PDCD4 axis. Our results indicate that high level of ANRIL may sharpen the degree of SCI via targeting miR-499a/PDCD4 axis to regulate the briskness of PI3K/Akt/mTOR/p70S6K signals.