RESUMEN
BACKGROUND: Ischemic stroke (IS) is a highly prevalent type of stroke with very high rates of disability and death. As the regulatory role of circular RNAs (circRNAs) in various diseases has been revealed, we constructed a stroke cell model to analyze the action mechanism of hsa_circ_0005548 in IS. METHODS: The abundance of hsa_circ_0005548, microRNA-362-3p (miR-362-3p) and E26 transformation specific-1 (ETS-1) were measured by real-time quantitative polymerase chain reaction (RT-qPCR) or western blot. We constructed an IS cell model in vitro by oxygen-glucose deprivation/reperfusion (OGD/R) treatment and analyzed cell proliferation, apoptosis and inflammatory response through the use of Cell Counting Kit-8 (CCK8), 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry and Enzyme-linked immunosorbent assay (ELISA), respectively. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were employed for the analysis of the relationship between miR-362-3p and hsa_circ_0005548 or ETS1. RESULTS: The higher abundance of hsa_circ_0005548 and ETS-1 and lower level of miR-362-3p were observed in human brain microvascular endothelial immortalized (HBMEC-IM) cells under OGD/R. Hsa_circ_0005548 downregulation mitigated OGD/R-induced HBMEC-IM cell injury. Mechanistically, hsa_circ_0005548 targeted miR-362-3p. MiR-362-3p knockdown reversed the effect of hsa_circ_0005548 silencing on OGD/R-induced HBMEC-IM cell injury. ETS1 was validated as a direct target of miR-362-3p, and miR-362-3p attenuated OGD/R-induced HBMEC-IM cell injury by ETS1. Moreover, hsa_circ_0005548 modulated ETS1 via miR-362-3p. CONCLUSION: Hsa_circ_0005548 knockdown repairs OGD/R-induced HBMEC-IM cell damage via miR-362-3p/ETS1 axis.
RESUMEN
A number of long non-coding RNAs (lncRNAs) have been identified to play an important role in the initiation and progression of glioma, including the stemness, survival, apoptosis, invasion, and drug resistance. However, the complex regulatory mechanisms of lncRNAs have not been well understood in glioma. Emerging evidence has confirmed that lncRNAs may act as a competing endogenous RNA (ceRNA) or a molecular sponge in modulating microRNAs (miRNAs), and the miRNAs negatively regulate target mRNA expression through complementarity binding to the 3'-untranslated region (3'UTR) of their target mRNAs. These interactions constitute complex signaling pathways in glioma, such as the lncRNAs/miRNAs/Wnt/ß-catenin pathway, the lncRNAs/miRNAs/PI3K/AKT/mTOR pathway, the lncRNAs/miRNAs/Notch pathway, the lncRNAs-miRNAs/MAPK kinase pathway, and the lncRNAs/miRNAs/NF-κB pathway. In this review, the underlying roles and molecular mechanisms of the lncRNAs and miRNAs pathway regulation network in glioma were summarized for a better understanding of tumorigenesis and pathogenesis of glioma.