CircPLXNB2 regulates acute myeloid leukemia progression through miR-654-3p/CCND1 axis

Abstract

ABSTRACTBackgroundAcute myeloid leukemia (AML) is a common hematological malignancy. Circular RNAs (circRNAs) are newly discovered endogenous non-coding RNAs that play important roles in regulating gene expression in cancer biology. The aim of this study was to identify novel prognostic and therapeutic targets associated with AML.MethodsThe expression levels of circRNA Plexin B2 (circPLXNB2), microRNA-654-3p (miR-654-3p) and cyclin D1 protein (CCND1) mRNA were detected by real-time quantitative polymerase chain reaction (qRT-PCR). The stability of circPLXNB2 was determined by RNase R and Actinomycin D assays. Cell counting kit-8 (CCK-8) and 5′-ethynyl-2′-deoxyuridine (EDU) assays were used to detect cell proliferation. Western blot was used to detect protein content. Cell apoptosis and cell cycle distribution were detected by flow cytometry. The relationship between miR-654-3p and circPLXNB2 or CCND1 was confirmed by dual-luciferase reporter assay.ResultsCircPLXNB2 was highly expressed in AML patients and cells, and circPLXNB2 was more stable than linear PLXNB2. Knockdown of circPLXNB2 affected the proliferation, apoptosis and cell cycle distribution of AML cells. CircPLXNB2 acted as a sponge for miR-654-3p and affected the progression of AML cells by targeting miR-654-3p. CCND1 was targeted by miR-654-3p, and miR-654-3p suppressed AML progression by targeting CCND1. CircPLXNB2 regulated CCND1 expression through sponging miR-654-3p.ConclusionIn conclusion, circPLXNB2 was highly expressed in AML patients and cells and modulated tumor progression by regulating the circPLXNB2/miR-654-3p/CCND1 axis, suggested that circPLXNB2 might be a new therapeutic target for AML treatment.