Spinal cord injury (SCI) is a devastating and common neurological disorder which causes local oxidative damage. The study aimed to investigate the underlying role of ANRIL in HO-induced cell injury of rat PC-12 cells. Cell injury was evaluated on the basis of cell viability, migration, invasion and apoptosis. The effect of ANRIL on HO-induced cell injury was estimated after cell transfection. Then, the interaction between ANRIL and miR-125a was explored by qRT-PCR and estimation of cell injury. Predicted by TargetScan, the possible target gene of miR-125a was verified. After that, the effects of aberrantly expressed target gene on cell viability, migration, invasion and apoptosis as well as phosphorylation of key kinases involved in JAK/STAT and ERK/MAPK pathways were evaluated. Results revealed that HO-induced PC-12 cell injury could be aggravated by ANRIL suppression. ANRIL appeared to act as a sponge of miR-125a, and ANRIL suppression promoted HO-induced cell injury by up-regulation of miR-125a. MCL-1 was a target of miR-125a, and MCL-1 was negatively correlated with miR-125a. Subsequent experiments showed the effect of MCL-1 silence on HO-induced PC-12 cell injury was the same as ANIRL suppression. MCL-1 attenuated HO-induced PC-12 cell injury by activating JAK/STAT and ERK/MAPK pathways. These findings suggested that knockdown of ANRIL aggravates HO-induced injury in PC-12 cells by targeting miR-125a. This might provide novel insights in the role of ANRIL in pathogenesis of oxidative damage during SCI.
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