The aim of the present study was to investigate the relative regulation of human circular RNA‑0054633 (hsa_circ_0054633), microRNA‑218 (miR‑218), roundabout 1 (ROBO1) and heme oxygenase‑1 (HO‑1) in human umbilical vein endothelial cells (HUVECs) in high glucose conditions. Initially, the expression of hsa_circ_0054633 in HUVECs was detected in high glucose conditions by reverse transcription‑quantitative polymerase chain reaction. Next, a small interfering RNA against hsa_circ_0054633 was constructed to investigate the function of jsa_circ_0054633 in HUVECs by transwell migration, cell counting kit‑8, flow cytometry and tube formation assays. In addition, the effect of hsa_circ_0054633 on the expression levels of ROBO1, HO‑1 and vascular endothelial growth factor were examined. The regulation effects of hsa_circ_0054633 on high glucose‑induced HUVEC proliferation, migration, and angiopoiesis were also analyzed. Bioinformatics analysis and dual‑luciferase assay were then used to confirm the direct or specific regulation of hsa_circ_0054633, miR‑218, ROBO1 and HO‑1. It was observed that high glucose levels increased the expression of hsa_circ_0054633, while downregulation of hsa_circRNA‑0054633 increased the high glucose‑induced endothelial cell dysfunction, including proliferation, migration and angiopoiesis suppression. Bioinformatics analysis revealed that the expression of circRNA‑0054633 was able to inhibit miR‑218 expression, which was clarified by the dual‑luciferase assay. It was also demonstrated that downregulating the expression of miR‑218 inhibited the high glucose‑induced endothelial cell dysfunction by promoting the expression of ROBO1 and HO‑1. These results suggest that the expression of hsa_circRNA‑0054633 has a protective effect against high glucose‑induced endothelial cell dysfunction by targeting ROBO1 and HO‑1.

Dysregulation of circular RNAs (circRNAs) has recently been found to play an important role in the progression and development of cancers such as non-small cell lung cancer (NSCLC). Yet the functions of many circRNAs in NSCLC remain unclear. In this study, the circRNA expression profiles in NSCLC tumor tissues and adjacent non-tumorous tissues were detected by high-throughput sequencing. Bioinformatics analyses, the dual-luciferase reporter system, fluorescence in situ hybridization (FISH) and miRNA/mRNA high-throughput sequencing were used to identify circ-EPB41 and its downstream target. The subcutaneous tumor/caudal vein transfer mouse model was used for tumor growth and invasion analysis. The results show that the circ-EPB41 was upregulated in NSCLC tissues and cell lines. Increased circ-EPB41 expression in NSCLC was significantly correlated with malignant characteristics, and positive to post-surgical overall survival of NSCLC patients. Reduced circ-EPB41 expression in NSCLC decreased cell proliferation and invasion in both in vitro and in vivo experiments. The miRNA/mRNA high-throughput sequencing suggested that downregulation of circ-EPB41 promoted microRNA (miR)-486-3p and suppressed eukaryotic translation initiation factor 5A (eIF5A) expression. Luciferase reporter experiments confirmed that miR-486-3p/eIF5A were downstream targets of circ-EPB41. In addition, we also found that downregulation of circ-EPB41 suppressed self-renewal and decreased expression of stemness markers SOX2, OCT-4, Nanog and CD133 by sponging miR-486-3p to enhance eIF5A expression. Taken togeter, these data revealed the important role of circ-EPB41 in regulating NSCLC cell invasion and proliferation by modifying miR-486-3p/eIF5A axis-mediated stemness. We believe our study provides a novel perspective regarding the role of circRNAs in NSCLC progression.

E2 promoter binding factor 1 (E2F1) has been reported to have an important regulatory role in cell survival during hyperglycemic conditions; however, the mechanisms remain to be fully elucidated. Bioinformatics analyses have suggested that microRNA (miR)‑17‑5p targets the 3'untranslated region (3'UTR) of E2F1. The aim of the present study was to characterize the protective effect of miR‑17‑5p/E2F1 on human umbilical vein endothelial cells (HUVECs) under high glucose (HG) conditions, to confirm the regulatory effect of miR‑17‑5p on E2F1/AMP‑activated protein kinase α2 (AMPKα2)‑mediated apoptosis and E2F1/mammalian target of rapamycin complex 1 (mTORC1)‑mediated autophagy. Bifluorescein experiments were performed to characterize the interaction between miR‑17‑5p and E2F1. The Cell Counting Kit‑8 assay, flow cytometry, immunofluorescence, and reverse transcription‑quantitative polymerase chain reaction and western blot analyses were used to detect cell viability, apoptosis, autophagy, and relative mRNA and protein expression, respectively. The results showed that HG induced the downregulation of miR‑17‑5p and upregulation of E2F1 during HUVEC injury. The downregulation of E2F1 inhibited HG‑induced HUVEC dysfunction by suppressing mTORC1‑mediated inhibition of autophagy and AMPKα2‑mediated promotion of apoptosis. The results suggested that inhibiting the expression of E2F1 protected against HG‑induced HUVEC injury via the activation of autophagy. The overexpression of miR‑17‑5p inhibited E2F1‑mediated HUVEC injury under HG conditions, which was reversed following transfection with an E2F1‑overexpression vector. The bifluorescein experiments showed that miR‑17‑5p targeted the 3'UTR of E2F1. Taken together, the results suggested that the expression of miR‑17‑5p inhibited HG‑induced endothelial cell injury by targeting E2F1.

The incidence of Klebsiella pneumoniae liver abscess (KPLA) has increased in a number of Asian countries over the past 30 years. Diabetes mellitus (DM) is a risk factor for KPLA. The prevalence and clinical features of KPLA in patients with and without DM have been well described; however, the underlying molecular mechanism responsible for the increased incidence of KPLA in patients with DM remains unclear. In the present study, a mouse model of DM was constructed and mice were infected with K. pneumoniae. Tissues were harvested for immunohistochemical and inflammatory factor expression analyses. The results revealed that the number of liver abscesses in mice with DM was greater than that observed in normal mice. The expression of interleukin (IL)‑1β, IL‑2, IL‑6, macrophage inflammatory protein‑1α and tumor necrosis factor‑α in the liver tissues of mice with DM was significantly higher compared with normal mice. Western blotting results revealed that the expression of phosphorylated (p)‑inhibitor of nuclear factor κΒ (NFκΒ) kinase subunit β, p‑NFκΒ and p‑inhibitor of NFκΒ was significantly increased in the liver tissue of mice with DM compared with that of normal mice. These results suggest that activation of the NFκΒ signaling pathways has a regulatory effect on the pathogenesis of K. pneumoniae bacteria liver abscesses and that high glucose conditions may promote the activation of NFκΒ signaling.