Identification the hub genes in HL-60 leukemia cells on decitabine through bioinformatics analysis

Abstract

Objective: Aims to identification the hub genes in HL-60 acute myeloid leukemia cells treated with decitabine, provide meaningful insights into the pathogenesis of AML. Methods: The gene expression profile of GSE24224 was obtained from GEO database, GO and pathway enrichment were performed though DAVID, established a PPI network from the STRING database and was displayed through the weight network diagram of omicShare tools. MiRNA targets and RBP targets prediction were carried out to further unravel the functions of hub genes identified. Results: 1558 differentially expressed genes were identified. GO and pathway analyses mainly involved citrulline metabolic process, positive regulation of neutrophil extravasation, positive regulation of cell adhesion molecule production, phospholipase A2 inhibitor activity, hematopoietic cell lineage, TGF-β signaling pathway, p53 signaling pathway. The miRNA and RBP targets prediction hinted that the 10 hub genes identified plays an important role in prognosis of AML. Conclusion: This study intimated that hub genes C3, C3AR1, FPR2, GNA11, PTAFR, ITGAM, ANXA1, LPAR1 CXCR4 and FPR1 identified predictively targeted hsa-miR-520d-5p, hsa-miR-362-5p, hsa-miR-224-5p, hsa-miR-1913, hsa-miR-196b-5, hsa-miR-188-5p, hsa-miR-130a-5p, hsa-miR-204-5p, hsa-miR-211-5p, hsa-miR-671-5p, hsa-miR-296-3p and hsa-miR-23b-3p and ADAR1, DGCR8, DKC1, ELAVL1, FBL, FUS, HNRNPC, IGF2BP2, NOP58, TAF15, U2AF2 and UPF1 proteins may regulate the occurrence and development of AML. This study provides meaningful insights and ideas for further understanding the pathogenesis of AML.