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neo_2018_181215N972

Title: LncRNA KCNQ1OT1 controls cell proliferation, differentiation and apoptosis by sponging miR-326 to regulate c-Myc expression in acute myeloid leukemia
Author: P. Cheng, P. Lu, J. Guan, Y. Zhou, L. Zou, X. Yi, H. Cheng

Abstract: Long noncoding RNAs (lncRNAs) have been reported to play essential roles in development and treatment of acute myeloid leukemia (AML). However, the role of lncRNA potassium voltage-gated channel subfamily Q member 1 overlapping transcript 1 (KCNQ1OT1) in AML progression and its mechanism remain largely unknown. The expressions of KCNQ1OT1, microRNA-326 (miR-326) and c-Myc were measured by quantitative real-time polymerase chain reaction and western blot, respectively. Phorbol myristate acetate (PMA) was used for cell differentiation. Cell proliferation, apoptosis and differentiation were measured by MTT assay, flow cytometry and qRT-PCR, respectively. The interaction between miR-326 and KCNQ1OT1 or c-Myc was explored by luciferase activity, RNA immunoprecipitation or RNA pull-down assay. We found the expression of KCNQ1OT1 was enhanced in AML samples compared with control. KCNQ1OT1 knockdown inhibited cell proliferation but promoted apoptosis and cell differentiation. KCNQ1OT1 was a decoy of miR-326 and c-Myc was a target of miR-326. KCNQ1OT1 regulated AML cell proliferation, apoptosis and differentiation by sponging miR-326. Moreover, overexpression of miR-326 suppressed proliferation but promoted apoptosis and PMA-induced differentiation by targeting c-Myc in AML cells. Besides, c-Myc protein level was suppressed by KCNQ1OT1 interference and rescued by miR-326 abrogation. Our data showed that KCNQ1OT1 regulates proliferation, differentiation and apoptosis in AML cells by acting as a competing endogenous RNA (ceRNA) for miR-326 to regulate c-Myc, providing a novel avenue for AML treatment.

Keywords: acute myeloid leukemia, KCNQ1OT1, miR-326, c-Myc, proliferation, differentiation
Published online: 07-Aug-2019
Year: , Volume: , Issue: Page From: , Page To:
doi:10.4149/neo_2018_181215N972


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