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Background: Long non-coding RNAs (lncRNAs) play important roles in the progression of glioma. Here, we examined the potential functions of a lncRNA, LINC01003, in glioma and characterized the underlying molecular mechanisms. Methods: The GEIPA2 and Chinese Glioma Genome Atlas (CCGA) databases were employed to analyze gene expression and the overall survival curve in patients with glioma. The functions of LINC01003 in glioma growth and migration were assessed by loss-of-function experiments in vitro and in vivo. RNA sequencing was used to determine the signaling pathways effected by LINC01003. Bioinformatics analysis and RNA immunoprecipitation (RIP) assays were used to explore the mechanism underlying the N6-methyladenine (m6A) modification-dependent upregulation of LINC01003 in glioma. Results: LINC01003 expression was upregulated in glioma cell lines and tissues. Higher LINC01003 expression predicted shorter overall survival time in glioma patients. Functionally, LINC01003 knockdown inhibited the cell cycle and cell proliferation and migration in glioma cells. Mechanistically, RNA sequencing revealed that LINC01003 mediated the focal adhesion signaling pathway. Furthermore, LINC01003 upregulation is induced by m6A modification regulated by METTL3. Conclusion: This study characterized LINC01003 as a lncRNA that contributes to tumorigenesis in glioma and demonstrated that the LINC01003-CAV1-FAK axis serves as a potential therapeutic target for glioma. [ABSTRACT FROM AUTHOR]

Background: Micro RNA (miRNA) plays important roles in macrophage polarization. However, the manner in which miRNA regulate macrophage polarization in response to dermatophagoides farinae protein 1(Der f1)-induced asthma has not been defined. This study aims to explore the role of miRNAs in regulating macrophages in asthma. Methods: The microRNAs which may regulate asthma were selectd by Microarrays. The function of miR-125b-5p in macrophage and Der f1-induced asthma were detected in vivo experiment. The long non coding RNA (lncRNA) AK089514/miR-125b-5p/TRAF6 axis was predicted by bioinformatics and confirmed by dual luciferase reporter assay. Results: In this study, we found that miR-125b-5p is highly expressed in M2 macrophages and bronchoalveolar lavage fluid (BALF) cells with Der f1-induced asthma. In response to the challenge of Der f1, miR-125b-5p KD attenuated allergic airway inflammation of mice by preventing M2 macrophages polarization. Mechanistic studies indicated that lncRNA AK089514 functioned as a competing endogenous RNA for miR-125b-5p, thereby leading to the depression of its endogenous target TNF receptor associated factor 6 (TRAF6). Conclusions: miR-125b-5p is significantly over-expressed in asthma, and AK089514–miR-125b-5p–TRAF6 axis play critical role in asthma by modulating macrophage polarization. Our findings may provide a potential new target for potential therapeutic and diagnostic target in asthma. [ABSTRACT FROM AUTHOR]

• LncRNA SLC8A1-AS1 is up-regulated in glioma. • Knockdown of lncRNA SLC8A1-AS1 inhibited glioma cell proliferation in vitro. • LncRNA SLC8A1-AS1 regulated glioma cell invasion and migration in vitro. • Down-regulation of lncRNA SLC8A1-AS1 suppressed glioma cell Wnt/β-catenin pathway. • Silencing of lncRNA SLC8A1-AS1 repressed glioma growth in vivo. As the most common aggressive malignant tumor in the central nervous system, glioma is still an insurmountable disease in the neural system. The mechanism of carcinogenesis in glioma remains largely unclear. In the present study, we identified a dysregulated long non-coding RNA (lncRNA) solute carrier family 8 member A1 antisense RNA 1 (SLC8A1-AS1) associated with glioma based on The Cancer Genome Atlas (TCGA) data. A validation experiment was conducted to confirm a high expression level of lncRNA SLC8A1-AS1 in glioma tissues. Down-regulation of lncRNA SLC8A1-AS1 suppressed the proliferation, colony formation, migration, and invasion of glioma cells in vitro and in vivo. Moreover, lncRNA SLC8A1-AS1 silencing decreased the activity of the Wnt/β-catenin pathway and suppressed the epithelial to mesenchymal transition (EMT) in glioma cells. These findings collectively provide novel insights into the function and mechanism of lncRNA SLC8A1-AS1 in the pathogenesis of glioma and highlight its potential as a therapeutic target for glioma intervention. [ABSTRACT FROM AUTHOR]

Obesity is a complicated metabolic disease characterized by meta-inflammation in adipose tissues. In this study, we explored the roles of a new long non-coding RNA (lncRNA), HEM2ATM, which is highly expressed in adipose tissue M2 macrophages, in modulating obesity-associated meta-inflammation and insulin resistance. HEM2ATM expression decreased significantly in adipose tissue macrophages (ATMs) obtained from epididymal adipose tissues of high-fat diet (HFD)-induced obese mice. Overexpression of macrophage HEM2ATM improved meta-inflammation and insulin resistance in the adipose tissues of HFD-fed mice. Functionally, HEM2ATM negatively regulated the production of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in macrophages. Mechanistically, HEM2ATM bound to heterogeneous nuclear ribonucleoprotein U (hnRNP U), suppressed hnRNP U translocation from the nucleus to the cytoplasm, hindered the function of cytoplasmic hnRNP U on TNF-α and IL-6 mRNA stabilization, and decreased the secretion of TNF-α and IL-6. Collectively, HEM2ATM is a novel suppressor of obesity-associated meta-inflammation and insulin resistance. [ABSTRACT FROM AUTHOR]