LncRNA DLGAP1 antisense RNA 2 (DLGAP1-AS2) is one kind cytoplasmic long non-coding RNA; however, there is rarely little information about its function in physiological process. Here, we demonstrated that LncRNA DLGAP1-AS2 was up-regulated in glioma and was quite correlated with poor prognosis of glioma patients. Depletion of DLGAP1-AS2 in glioma cells could inhibit cell proliferation and cell migration, and induce cell apoptosis, resulting in the suppression of the progression of glioma consequently. Furthermore, knockdown of DLGAP1-AS2 inhibited the growth of xenograft glioma tumour in vivo as well. Finally, we verified Yes Associated Protein 1 (YAP1) was the downstream target of DLGAP1-AS2 and DLGAP1-AS2 modulated glioma cell proliferation, migration and apoptosis via regulating YAP1. Our study revealed novel mechanism about how did lncRNA DLGAP1-AS2 execute function in glioma and thus provided potential therapeutic interventions for the treatment of glioma.

Stroke recovery is associated with neural stem cell (NSC) development and neurovascular unit reconstruction. The exosome, as an important intercellular player in neurovascular communication, mediates neuro-restorative events by transferring exosomal protein and RNA cargoes. In this study, we explored the role of exosomal microRNAs (miRNAs) in human NSCs (hNSCs), and analyzed the expression profiles of miRNAs in hNSC-derived and hypoxic preconditioning hNSC-derived exosomes with the help of next generation sequencing (NGS). The results demonstrated that a certain proportion of miRNAs were differentially expressed in both exosomes. In addition, target gene prediction and Gene Ontology (GO) enrichment analysis showed that these genes were associated with differential miRNAs primarily participating in biological processes (regulation of cellular process), cellular component (intracellular membrane-bounded organelle), and molecular function (binding). Kyoto Encyclopedia of Genes and Genomes pathway (KEGG) pathway enrichment data suggested that most of targeted genes involved in PI3K-Akt, Hippo, MAPK, mTOR, and Endocytosis etc. signaling pathways. We identified the interesting and important expressed miRNA and considered that miR-98-3p might be a special hNSC-derived exosomal-miRNA which was significantly downregulated under hypoxic preconditioning. The hNSCs-derived exosomes were capable of modulating gene expression or promoting stroke therapy. We observed that after hypoxic preconditioning, the functions of these exosomes were changed, and exosomal-miRNAs expression profile was different. In summary, our study suggested that hNSC-derived exosomal miRNAs including hypoxic preconditioning exosomal miRNAs provided a new strategy for the diagnosis and treatment of stroke patients.

Gliomas are a group of heterogeneous primary central nervous system tumors arising from glial cells. These tumors are associated with high morbidity and mortality. New opportunities for the development of effective therapies for malignant gliomas are urgently needed. Magnetic nano-particles can heat up tumor tissues and induce the killing of cancer cells. However, the in vivo action of magnetic nano-iron hyperthermia on brain gliomas has not been widely investigated. The safety, efficacy, and suitable dose of hyperthermia therapy remain unknown. We successfully established a rat model of brain glioma by injecting C6 glioma cells into the right caudate nuclei of rats. Fixed doses (2.5, 5, or 10 mg) of magnetic nano-iron were then injected into the tumors of tumor-bearing rats. The survival time of tumor-bearing rats was subsequently observed, and imaging studies were conducted on the brain tumors. Of the 80 rats that underwent C6 glioma cell implantation, 70 exhibited decreased mobility and appetite, and wasting. Establishment of this brain glioma model was confirmed to be successful by magnetic resonance imaging. After injection of different doses of magnetic nano-iron, the survival times of the different dose groups of tumor-bearing rats were not significantly different. However, the tumor size exhibited a significant decrease with magnetic nano-iron hyperthermia therapy. Injection of various doses of magnetic nano-iron was safe in tumor-bearing rats. The effective doses were 2.5 and 5 mg. Magnetic nano-iron hyperthermia significantly shrank the brain gliomas in tumor-bearing rats.

Inflammatory response generated by ischemic stroke commonly affects functional or structural recovery. The aim of this study was to examine the IFN-γ caused inflammatory effects on NSCs in vitro and in vivo. We found that IFN-γ did not affect NSCs proliferation but increased the SOD2 level of inflammatory oxidative stress in NSCs culturing. High dose IFN-γ (500 ng) injection aggravated the level of inflammation in the cerebral ischemic model but did not alter the repairing functions of the NSCs in vivo. NSCs based treatment, including the NSCs-IFN-γ combined treatment, significantly improved the ischemic microenvironment by decreasing CD4+, CD8+ T cells and microglia infiltration. Furthermore, anti-inflammatory cytokines IL-10 and TGF-β1 expression were increased in the NSCs and combined treatment groups, but the level of pro-inflammatory cytokines (IL-1 β, IL-6, IFN-γ, and TNF-α) were decreased. The IFN-γ/Stat1 signaling pathway was also activated. NSCs transplantation therefore promoted the neurological recovery of ischemic stroke rats mainly by altering the inflammatory microenvironment, neutralizing the negative effect of IFN-γ. In conclusion, in addition to promoting cell replacement or engraftment, the NSCs-based transplantation also enhanced the therapeutic effects of transplantation by optimizing its immune microenvironment of ischemic areas.

Previous studies have reported that miRNAs are involved in the progression of glioma, and that miR-27b-3p is involved in a variety of cancers. However, whether miR-27b-3p has a role in glioma is still unknown. Here, we demonstrated that miR-27b-3p is downregulated in glioma, and this is associated with the development of glioma. Overexpression of miR-27b-3p in glioma cells inhibits cell proliferation and migration, and induces cell apoptosis, which suppresses the progression of glioma. Furthermore, in our study, overexpression of miR-27b-3p also inhibited the growth of xenografted glioma tumors in-vivo. Finally, we verified that Yes Associated Protein 1 (YAP1) is the downstream target of miR-27b-3p, and that miR-27b-3p controls the proliferation, migration, and apoptosis of glioma cells via regulating YAP1. Our study reveals a novel mechanism through which miR-27b-3p functions in the development of glioma, and thus provides a potential therapeutic target for the treatment of glioma.