KIF11 serves as a cell cycle mediator in childhood acute lymphoblastic leukemia

Abstract

Abstract The extremely high incidence and mortality of ALL remain to a great threat to children worldwide. This study aims to explore a novel biomarker for childhood ALL based on the analysis using the Gene Expression Omnibus (GEO) database. Array data of the GSE73578 dataset, involving 46 childhood ALL samples, were downloaded from the GEO database. The weighted gene co-expression network analysis (WGCNA) was performed to explore co-expression modules associated with childhood ALL. The functions of hub module associated with many vital processes were also predicted by Gene Ontology (GO) and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway enrichment analysis. The KIF11 gene was screened out by overlapping down-regulated genes in GSE73578 and GSE4698 datasets and the hub module. Guilt by association (GBA) was adopted to verify the function of the identified KIF11 gene and to predict its target genes associated with the treatment of childhood ALL. KIF11 was up-regulated in bone marrow samples of childhood ALL patients and corresponding cell lines. Furthermore, in vitro experiments confirmed that knockdown of KIF11 in ALL cells inhibited cell proliferation and arrested cell cycle progression in G2/M phase. We identified KIF11 as a therapeutic marker for childhood ALL. Our study provides references for elucidating the molecular mechanism underlying the pathogenesis of childhood ALL.