Department of Neurosurgery, The Second Xiangya Hospital, Central South University, Changsha, China,
Published: September 2020
AI Article Synopsis
Article Abstract
Background: Glioma is identified as a broad category of brain and spinal cord tumors. MiR-362-3p is important in regulating the genesis of different cancers; however, the mechanism of miR-362-3p in the progression of glioma remains largely unknown.
Objectives: This study aimed to elucidate pathobiological functions of miR-362-3p by targeting PAX3 in glioma.
Method: qRT-PCR and western blotting were used to examine miR-362-3p and PAX3 expression in glioma tissues and cells. CCK-8 assay and transwell assays were used to examine the functions of miR-362-3p on human glioma. Two bioinformatics analysis software and luciferase reporter assay were performed to analyze the relationship between miR-362-3p and PAX3.
Results: MiR-362-3p was downregulated, and PAX3 was upregulated in glioma tissues and cells. Functional assays revealed that ectopic expression of miR-362-3p inhibited glioma cell proliferation and migration. Further, PAX3 was confirmed as direct target gene of miR-362-3p, and downregulation of PAX3 reversed the suppressive effects of miR-362-3p in glioma. In addition, miR-362-3p also exhibited suppressive effect on epithelial-mesenchymal transition and Wnt/β-catenin pathway.
Conclusions: MiR-362-3p downregulation or PAX3 overexpression predicted poor prognosis in glioma. MiR-362-3p played a role in the suppressive effect on glioma by targeting PAX3 through suppressing Wnt/β-catenin pathway.
Department of Intravenous Drug Dispensing, Zibo Central Hospital, No. 54, Gongqingtuan West Road, Zhangdian District, Zibo City, 255020, Shandong Province, China.
The study investigates how Astragaloside IV (AS IV) protects against lung injury and pulmonary fibrosis caused by PM2.5 in a rat model.
Results show that AS IV reduces lung tissue damage, inflammation, and cell death in both the rat model and alveolar epithelial cells exposed to PM2.5.
The mechanism involves AS IV upregulating miR-362-3p, which inhibits RUNX1 expression, enhancing the protective effects of AS IV against PM2.5-induced lung injury.
MicroRNAs can be regarded as biomarkers for gastric cancer (GC) diagnosis in the early stages. This study assesses the expression levels of miR-362-3p, miR-362-5p and miR-363-5p as potential biomarkers for GC. The expression levels of the miRNAs in 90 pairs of GC and adjacent normal tissue samples were analyzed by quantitative real-time reverse transcription PCR (qRT-PCR) and some bioinformatics tools were utilized for analyzing the target genes and possible molecular pathways in which these miRNAs participate.
To investigate the effects and the related signaling pathway of miR-362-3p on OS. The bioinformatics analysis approaches were employed to investigate the target pathway of miR-362-3p. After the 143B and U2OS cells and nu/nu male mice were randomly divided into blank control (BC) group, normal control (NC) group, and overexpression group (OG), the CCK-8, EdU staining, wound healing assay, Transwell assay, and TUNEL staining were adopted to respectively determine the effects of overexpressed miR-362-3p on the cell viability, proliferation, migration, invasion, and apoptosis of 143B and U2OS cells , tumor area assay and hematoxylin and eosin staining were employed to respectively determine the effects of overexpressed miR-362-3p on the growth and pathological injury of OS tissue .
