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Abstract
Background
The regulatory potency of circular RNA (circRNA) has been acknowledged in multiple human diseases, including ischaemic stroke (IS). However, only a few circRNAs were investigated in this disorder. We aimed to uncover the role of circ_0001360 in cell models of IS in vitro.
Methods
SK-N-SH cells were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) to simulate IS pathology conditions in vitro. Quantitative real-time PCR (qPCR) and western blot were applied for expression detection. Cell viability, proliferation and apoptosis were investigated by CCK-8, EdU and flow cytometry assays. The predicted binding of miR-671-5p to circ_0001360 or BMF 3’UTR was validated by dual-luciferase reporter and RIP assays. Proteins on the NF-κB pathway were quantified by western blot to assess NF-κB pathway activity.
Results
Circ_0001360 was upregulated in SK-N-SH cells after OGD/R treatment. OGD/R provoked SK-N-SH cell growth impairment, apoptosis and inflammation, while circ_0001360 knockdown relieved these injuries. Circ_0001360 targeted miR-671-5p, and miR-671-5p deficiency recovered SK-N-SH cell injury that was repressed by circ_0001360 knockdown. MiR-671-5p directly combined with BMF and repressed BMF expression. Accordingly, circ_0001360 targeted miR-671-5p to regulate the expression of BMF. Circ_0001360 knockdown weakened the phosphorylated levels of P65 and IκBα, while further miR-671-5p deficiency or BMF overexpression restored their expression levels.
Conclusion
Circ_0001360 contributed to OGD/R-caused SK-N-SH cell injury via targeting the miR-671-5p/BMF network and activating the NF-κB pathway, thus participating in the development of IS.
Disclosure statement
The authors declare that they have no conflicts of interest.
Funding
The author(s) reported there is no funding associated with the work featured in this article.