Members of the GATA‑binding factor protein family, including GATA1, GATA2 and GATA3, serve an inhibiting role in leukemia. The present study demonstrated that GATA4 was upregulated in children with acute lymphoblastic leukemia (ALL). Results from a number of functional experiments, including cell proliferation analysis, cell cycle analysis, cell apoptosis assay and Transwell migration and invasion analyses, have suggested that high expression of GATA4 may facilitate proliferation and metastasis, and suppress apoptosis in ALL cells. Chromatin immunoprecipitation assay and luciferase reporter assay revealed that GATA4 was a transcription factor that activated mouse double minute 2 homolog (MDM2) and B cell lymphoma 2 (BCL2) expression in ALL cells. BCL2 is a key anti‑apoptosis protein that was demonstrated to suppress cell apoptosis. In addition, GATA4 was revealed to regulate p53 through the transcriptional activation of MDM2, subsequently influencing cell cycle and apoptosis. Results from the present study suggested that GATA4 may be a key marker in ALL diagnosis and a potential target of molecular therapy.

There is a close relationship between acute asthma and autophagy. In addition, some studies claim that miR-146 can regulate autophagy and participate in acute asthma. This study further explores the role of miR-146 in acute asthma and underlying mechanism. Twenty BALB/c mice were selected and randomly divided into two groups, the model group and the control group, each with 10 mice. Lung tissues, peripheral blood, alveolar lavage fluid, and primary lymphocytes were separated into miR-146 over expression group (miR-146 mimic), miR-146 low expression group (miR-146 inhibitor), negative control group (NC), blank group, or SBI-0206965 group. Acute asthma was established and the expression levels of miR-146, EGFR, TLR4, LC3, beclin1, and ATG5 in each group was measured. The targeting relationship and correlation between miR-146 and EGFR were also investigated. The expression of IL-4 in model group was increased compared to control arm while the expression of IFN-γ was opposite (P < 0.05). The expressions of miR-146, LC3, beclin1, and the expression of ATG5 were decreased (P < 0.05). The expressions of miR-146 gene and LC3, beclin1, ATG5 mRNA and protein in the miR-146 mimic group were the highest, while the expressions of EGFR and TLR4 were the lowest. The SBI-0206965 group and the miR-146 inhibitor group are opposite to the miR-146 mimic group, the SBI-0206965 group and the miR-146 inhibitor group have significant differences (P < 0.05). miR-146 has a directly targeted EGFR and TLR4, and both showed a negative correlation (rEGFR=−0.397, P = 0.013; rTLR4=−0.402, P = 0.021). During the onset of asthma, miR-146 was abnormally decreased. miR-146 directly targets and negatively regulates EGFR. In addition, miR-146 down-regulates TLR4 gene to increase CD4+ lymphocytes’ aphagocytosis-related markers (LC3, beclin1, ATG5) which further promotes the autophagy process and ultimately alleviates the degree of acute asthma. Its main mechanism is related to the down-regulation of the EGFR/TLR4 through regulated the expression of autophagy. Our study provided a scientific reference for further understanding of acute pathogenesis of asthma.