Effect of multitargeted kinase inhibitor GNF-7 on the expression profiling of leukemia cell lines
10.13699/j.cnki.1001-6821.2018.03.034
- VernacularTitle:多靶点激酶抑制药GNF-7对白血病细胞表达谱的影响
- Author:
Ling-Hua JING
1
;
Song-Nian LIU
;
Hai-Ping YANG
;
Lin-Hai RUAN
Author Information
1. 河南科技大学临床医学院、河南科技大学第一附属医院血液科
- Keywords:
leukemia;
targeted treatment;
kinase inhibitor;
cell apoptosis;
bioinformatics
- From:
The Chinese Journal of Clinical Pharmacology
2018;34(3):300-303
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effect of multitargeted kinase inhibitor GNF-7 on the expression profiling of leukemia cell lines.Methods The expression profiles dataset GSE49534 was downloaded from the Gene Expression Omnibus (GEO) database.The BRB-Array Tools software package was employed to screen the differentially expressed genes (DEGs),then the Gene Ontology (GO) function,pathway enrichment,gene interaction network,and pathway relation network analyses were conducted based on these differential genes.Results Totally,847 differential genes were screened out,of which 426 genes were up-regulated and 419 genes were down-regulated.GO enrichment analysis showed that DEGs mainly performed the molecular functions of binding,protein kinase activity,and signal transducer activity,and participated in biological process of signal transduction,small molecule metabolic process,and apoptotic process.The pathway analysis found that DEGs were mostly enriched in ribosome biogenesis in eukaryotes,metabolic pathways,Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway,etc.The network analyses mining identified the hub genes,which included polyribonucleotide nucleotidyltransferase 1 (PNPT1),adenylate kinase 4 (AK4),Janus kinase 2 (JAK2),signal transducer and activator of transcription 2 (STAT2),MYC;and core pathways such as mitogen-activated protein kinase (MAPK) signaling pathway,apoptosis,cell cycle,pathways in cancer.Conclusion The GNF-7 inhibited leukemia cells via induction of apoptosis and cell cycle arrest.
