miR-1290 PROMOTES PROLIFERATION AND SUPPRESSES APOPTOSIS IN ACUTE MYELOID LEUKEMIA BY TARGETING FOXG1/SOCS3

Abstract

Acute myeloid leukemia (AML) is an invasive hematological malignancy of which the mechanismis still unknown. MicroRNAs (miRNAs) act as critical controllers of target gene expression at posttranscriptionallevel. MiR-1290 is found to abnormally express in multiple cancers, however, its rolein AML is still unknown. In this study, the mRNA and protein expression levels of related genes weredetermined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Westernblot. Luciferase assay was used to verify the target genes of miR-1290. In addition, the cell proliferation,cell cycle and apoptosis of HL-60 and KG-1 cells were detected by Counting Kit-8 (CCK-8) and flowcytometry assay, respectively. Our results showed that the expression of miR-1290 was increased inAML in vivo and in vitro. Gain and loss of function experiments by transfection of miR-1290 mimicsor miR-1290 inhibitors into HL-50 and KG-1 cells indicated that miR-1290 significantly promoted cellproliferation and inhibited cell apoptosis. Furthermore, Forkhead-box gene 1 (FOXG1) and Suppressorof cytokine signaling 3 (SOCS3) were verified to be the target genes of miR-1290. Overexpression ofFOXG1 or SOCS3 inhibited cell proliferation and induced cell apoptosis in HL-50 and KG-1 cells.Moreover, knockdown of miR-1290 inhibited cell proliferation and promoted apoptosis, whereas theseeffects were reversed by silencing of FOXG1 or SOCS3 in HL-50 and KG-1 cells. In conclusion, miR-1290 promoted proliferation and suppressed apoptosis in AML by targeting FOXG1 and SOCS3, whichmight provide a therapeutic target for AML.