Gene expression profiles and protein-protein interaction networks in neuroblastoma with MEIS2 depletion.

PURPOSE: The purpose of the present study was to identify differential gene expressions (DEGs) and key pathways in neuroblastoma with MEIS2 depletion through bioinformatics. METHODS: The microarray gene expression dataset GSE56003 was downloaded from the Gene Expression Omnibus (GEO) database. DEGs were identified using Gene Level RMA sketch and Transcriptome Analysis Console. Gene ontology (GO) function and KEGG pathway enrichment analysis of DEGs were performed using the DAVID online tool. Protein-protein interaction (PPI) networks were constructed by mapping the DEGs onto Cytoscape software. MCODE algorithm was used to select the module and Centiscape was used to screen the hub genes. The Kaplan-Meier survival curves was utilized to show the correlation of specific gene expressions and the survival situation of NB patients. Results：A total of 1352 DEGs were identified in neuroblastoma with MEIS2 depletion, which were mainly enriched during the cell cycle, DNA replication, and DNA repair. CDK2, RAD51, BRCA1, and MCM3 were selected as hub genes that have the potential as novel therapeutic targets for neuroblastoma. CONCLUSION: This study revealed the hub genes and pathway involved in neuroblastoma with MEIS2 knockdown, which offered new insights into the molecular networks underlying MEIS2 depletion in neuroblastoma. Additionally, this study provided a valuable resource of potential biomarkers and therapeutic targets.

The effect of astragalin on the VEGF production of cultured Müller cells under high glucose conditions.

Diabetic retinopathy (DR) is a severe complication of diabetes mellitus (DM) and often causes vision loss or even blindness. Vascular endothelial growth factor (VEGF) in the retina, which is mainly derived from Müller cells, is a crucial biological factor in the development of DR. Astragalin is extracted from Astragalus membranaceus and has many pharmacological properties. Studies showed that astragalin has beneficial effects on hyperglycemia. To evaluate the effect of astragalin in preventing and treating DR and determine astragalin's mechanism of action, Müller cells were collected from rat retina, cultured in vitro and identified using immunocytochemistry. They were divided into four groups: the high glucose group (20 mmol/l), the normal control group, the astragalin group (400 mg/l) and the high glucose (20 mmol/l) + astragalin (400 mg/l) group. After 3 days of treatment, immunocytochemical and reverse transcription-polymerase chain reaction (RT-PCR) analysis of VEGF was carried out. Our results demonstrated that astragalin decreased the overexpression of VEGF in Müller cells and alleviated the effects caused by high glucose. Thus, astragalin has promising application in preventing and treating DR caused by DM.