LncRNA KIAA0125 promotes the proliferation of Kasumi-1 cells through the miR-4640-5p/KCNQ1 axis with associated changes in the Wnt/β-catenin signaling pathway

To investigate the effects of the long non-coding RNA (lncRNA) KIAA0125 on the proliferation and apoptosis of the human acute myeloid leukemia subtype M2 (M2-AML) cell line Kasumi-1. Recombinant lentivirus technology and CRISPR/Cas9-SAM technology were used to construct Kasumi-1 cells with downregulated or overexpressed lncKIAA0125, respectively. The cell proliferation rate of each group was determined using the cell counting kit-8 (CCK-8) assay, and the apoptosis rate was determined via flow cytometry. The binding between miR-4640-5p and lncKIAA0125, and between miR-4640-5p and KCNQ1, was subsequently verified using RIP and dual-luciferase assays. Western blotting was used to detect proteins related to the Wnt/β-catenin signaling pathway in each group, and rescue experiments were performed to confirm the role of the lncKIAA0125/miR-4640-5p/KCNQ1 axis in Kasumi-1 cells. Finally, a subcutaneous xenograft tumor model was established to verify the effect of lncKIAA0125 on the growth of Kasumi-1 cells in vivo. Downregulation of lncKIAA0125 inhibited Kasumi-1 cell proliferation and promoted apoptosis, whereas upregulation of lncKIAA0125 had the opposite effect on cell proliferation. RIP and dual-luciferase assays confirmed that lncKIAA0125 directly bound to miR-4640-5p and that miR-4640-5p also bound to KCNQ1. Moreover, downregulation of lncKIAA0125 inhibited KCNQ1 expression at both the mRNA and protein levels and reduced signaling related to the Wnt/β-catenin pathway. Conversely, upregulation of lncKIAA0125 produced the opposite effects. Finally, in vivo findings demonstrated that downregulating lncKIAA0125 expression suppressed the proliferation of Kasumi-1 cells in nude mice. lncKIAA0125 is highly expressed in AML cells and appears to promote the proliferation of Kasumi-1 cells via the miR-4640-5p/KCNQ1 axis and was associated with changes in the Wnt/β-catenin signaling pathway.