Conclusion
Decreased expression of circMYC could suppress AML progression by regulating miR-516a-5p/AKT3, suggesting a new therapeutic target in AML treatment.
Methods
Expression levels of CircMYC, miR-516a-5p, AKT3 and apoptosis-related proteins were determined by RT-qPCR and western blot. Cell viability and proliferation were examined by CCK8 assay and EdU assay. Annexin V/PI staining was used to assess cell apoptosis. Mitochondrial respiration function was confirmed by oxygen consumption rate (OCR). The relationships among circMYC, miR-516a-5p and AKT3 were detected by dual-luciferase reporter (DLR) assay, RNA-pull down assay and RNA immunoprecipitation (RIP) assay, respectively.
Objective
Acute myeloid leukemia (AML) is a hematological malignancy with an aberrant proliferation of immature myeloid cells. This study aimed at exploring the regulatory function of circMYC in AML progression.
Results
CircMYC was positively correlated with poor prognosis in AML patients (all P<0.05). Knockdown of circMYC decreased cell viability and OCR but increased cell apoptosis rates (all P<0.05), and miR-516a-5p overexpression displayed the similar trend. Mechanistically, the oncogenic effects of circMYC were achieved by sponging miR-516a-5p and increasing AKT3.