RARRES1 is a novel immune-related biomarker in GBM.

Immunotherapy is a promising route for the treatment of glioblastoma (GBM). Researchers have conducted a large number of studies on the pathogenesis of GBM; however, these studies are not comprehensive. High-throughput sequence analysis allows for insights into the pathogenesis of GBM. In this study, we used The Cancer Genome Atlas dataset to identify the function of RARRES1 enriched in GBM, especially in the WHO grade-IV cases. We discovered that RARRES1 is highly expressed in patients with mesenchymal subtype, unmethylated MGMT, IDH1 wild type, and non-G-CIMP, all of which are molecular characteristics of malignant GBM. Results of the immune microenvironment analysis showed that RARRES1 is strongly correlated with dendritic cells PD1, PDL2, TIM3, and CTLA4, which are the immune checkpoints in GBM. Furthermore, according to the overall survival and status analysis, a high expression of RARRES1 was found to be an unfavorable factor for prognosis. This indicates that RARRES1 may participate in the pathogenesis and immune-related processes in GBM, and may serve as a therapeutic target.

Intranasal Delivery of Granulocyte Colony-Stimulating Factor Enhances Its Neuroprotective Effects Against Ischemic Brain Injury in Rats.

Granulocyte colony-stimulating factor (G-CSF) is a hematopoietic growth factor with strong neuroprotective properties. However, it has limited capacity to cross the blood-brain barrier and thus potentially limiting its protective capacity. Recent studies demonstrated that intranasal drug administration is a promising way in delivering neuroprotective agents to the central nervous system. The current study therefore aimed at determining whether intranasal administration of G-CSF increases its delivery to the brain and its neuroprotective effect against ischemic brain injury. Transient focal cerebral ischemia in rat was induced with middle cerebral artery occlusion. Our resulted showed that intranasal administration is 8-12 times more effective than subcutaneous injection in delivering G-CSF to cerebrospinal fluid and brain parenchyma. Intranasal delivery enhanced the protective effects of G-CSF against ischemic injury in rats, indicated by decreased infarct volume and increased recovery of neurological function. The neuroprotective mechanisms of G-CSF involved enhanced upregulation of HO-1 and reduced calcium overload following ischemia. Intranasal G-CSF application also promoted angiogenesis and neurogenesis following brain ischemia. Taken together, G-CSF is a legitimate neuroprotective agent and intranasal administration of G-CSF is more effective in delivery and neuroprotection and could be a practical approach in clinic.