AEBP1 Is Involved In The Study Of The Mechanism Of Regulation Of Childhood Acute Lymphoblastic Leukemia

Objective:Acute lymphoblastic leukemia(ALL)is a common malignancy among children and adolescents,which accounts for 35% of malignancy of children and is one of the main threaten for children healthy and life.With the development of medical technology,cALL treatment has been improved significantly in recent years,but the mechanism of it remains unclear.Methods:This study took GSE67684,GSE28460,and GSE60926 as the study objectives to screen cALL associated differentially expressed genes(DEGs)in GSE67684 and then integrated with cALL relapse associated DEGs to obtain cALL development and prognosis associated DEG-AEBP1.Subsequently,we took the AEBP1 as the breaking points to screen AEBP1 co-expressed DEGs with Pearson co-efficient followed by Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)functional enrichment analyses using DAVID online tool.To further reveal the biofunction of AEBP1,the expression of AEBP1 in different leukemia cell lines was detected and the appropriate cell line Jurkat was selected.Then,the expression of AEBP1 was silenced with shRNA followed by proliferation,apoptosis,and cell cycle analyses.Results:After integrative analysis for these three datasets,a total of 53 specific DEGs,including AEBP1 were obtained which were always downregulated in cALL after treatment but had no significant difference between diagnosis and relapse samples.Taking AEBP1 as the breaking points,AEBP1 expression associated DEGs were identified and subject for GO and KEGG functional enrichment analyses.The results showed that AEBP1 expression associated DEGs were significantly enriched in immune response,cell adhesion,blood coagulation,and cell surface cytokine receptor interaction associated functions and pathways,indicating that these genes had play critical role in these mechanism in cALL.Compared with normal Pbmc cells,expression of AEBP1 was significantly upregulated in Jurkat,Nalm-6,HL-60,and Raji cell lines,especially in Jurkat and HL-60 cells.shAEBP1 could significantly inhibit the proliferation of Jurkat cells and cell cycle transition from G1 phase to S phase.Silencing AEBP1 could significantly promote apoptosis and caspase-3/7 activity in Jurkat cells,as well as the expression of Bax,but inhibit the expression of p53 and Bcl-2.Conclusion:Expression of AEBP1 was significantly correlated with the pathogenesis and prognosis of cALL.Inhibiting the expression of AEBP1 in cALL cell lines could significantly attenuate the proliferation but promote apoptosis of tumor cells.Therefore,it is important to further explore the biofunction of AEBP1 in cALL based on the findings provided by bioinformatics,so that could provide some new information in cALL mechanism investigation and improve the clinical diagnosis and therapy of cALL.