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The apoptosis of vascular endothelial cells (VEC) is related to ischemic stroke. Phosphatidylinositol-3 kinase (PI3K)/protein kinase B (AKT/PKB) signaling pathway can upregulate Bcl-2 expression, reduce reactive oxygen species (ROS) production, and induce apoptosis. The level of miR-124 was significantly increased after cerebral ischemia. This study aimed to investigate the role of miR-124 in regulating PI3K expression, brain VEC apoptosis, and ROS production.The expressions of miR-124, PI3K, p-AKT, and Bcl-2 in brain VEC of rats from the sham group and middle cerebral artery occlusion (MCAO) group were tested. Bioinformatics analysis showed the complementary binding site between miR-124 and PI3K mRNA. ROS content and cell apoptosis were detected by flow cytometry. Rat brain VEC were cultured in vitro and treated by oxygen-glucose deprivation (OGD) for 6 h. VECs were divided into four groups, including miR-NC, miR-124 inhibitor, pIRES2-blank, and pIRES2-PI3K groups, and were further treated by OGD.MiR-124 expression, ROS content, and cell apoptosis were markedly increased, whereas the levels of PI3K, p-AKT, and Bcl-2 were markedly reduced in rat VECs from MCAO group compared with that in the sham group. OGD treatment significantly induced VECs apoptosis, upregulated miR-124 expression and ROS content, and down-regulated the levels of PI3K, p-AKT, and Bcl-2. MiR-124 inhibitor or transfection of pIRES2-PI3K plasmid apparently enhanced PI3K, p-AKT, and Bcl-2 expressions, alleviated cell apoptosis and decreased ROS content in VECs induced by OGD.Our data demonstrated that miR-124 induced the apoptosis of brain vascular endothelial cells via the down-regulation of PI3K/AKT signaling pathway and promotion of ROS production.

Many findings have demonstrated long noncoding RNAs (lncRNAs) as crucial regulatory molecules in the progression of osteosarcoma. The aim of this study was to explore the roles and mechanisms of LncRNA LINC00689 (LINC00689) in osteosarcoma.Differential levels of LINC00689 and miR-655 in osteosarcoma samples and cell lines were analyzed by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The associations between LINC00689 expression and prognostic significance of osteosarcoma patients were analyzed using a series of statistical assays. Loss-of-function and gain-of-function assays were performed to investigate the role of LINC00689 in proliferation and metastasis in vitro. Bioinformatic assays, Luciferase report assays, and rescue assays were applied to illustrate the ceRNA mechanism network of LINC00689/miR-655/SOX18.We found that LINC00689 expression was distinctly upregulated in osteosarcoma specimens and cell lines. MiR-655 displayed a trend of remarkably decreased expression in osteosarcoma tissues. In addition, we showed that LINC00689 could specifically interact with the promoter of SP1 and activate LINC00689 transcription. Further clinical studies indicated that higher levels of LINC00689 were associated with advanced clinical stage, positively distant metastasis, and unfavorable clinical outcome. Functional studies revealed that the knockdown of LINC00689 suppressed the proliferation, migration, and invasion of osteosarcoma cells, and promoted apoptosis. Final mechanistic investigations confirmed that upregulation of LINC00689 competitively bound to miR-655 that prevented SOX18 from miRNA-mediated degradation, thus facilitating osteosarcoma progression.All our findings suggested that SP1-induced upregulation of LINC00689 promoted osteosarcoma progression by regulating miR-655/ SOX18 axis, which provided a novel insight for osteosarcoma tumorigenesis.

Recently, long noncoding RNAs (lncRNAs) have attracted much attention for their roles in tumor progression. The aim of this study was to investigate the exact role of lncRNA OR3A4 in the development of ovarian cancer (OC), and to explore the possible underlying mechanism.OR3A4 expression in OC tissue samples was detected by Real-time quantitative polymerase chain reaction (qRT-PCR). Moreover, wound healing assay and transwell assay were performed to evaluate the effect of OR3A4 on the metastasis of OC. Furthermore, the underlying mechanism was explored by RT-qPCR and Western blot assay.The expression level of OR3A4 in OC samples was significantly higher than that of adjacent tissues. Moreover, cell migration and invasion were significantly repressed after OR3A4 knockdown in vitro. Moreover, the mRNA and protein expressions of kruppel-like factor 6 (KLF6) were remarkably upregulated after knockdown of OR3A4. Furthermore, the expression level of KLF6 was negatively correlated with the expression of OR3A4 in OC tissues.Our results showed that OR3A4 could enhance OC cell metastasis and invasion via suppressing KLF6. Moreover, OR3A4 might be a potential therapeutic target for OC.