CircMYC regulates the mitochondrial respiration and cell viability via miR-516a-5p/AKT3 axis in acute myeloid leukemia.

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. 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. 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. CONCLUSION Decreased expression of circMYC could suppress AML progression by regulating miR-516a-5p/AKT3, suggesting a new therapeutic target in AML treatment.