Long noncoding RNA NEAT1 modulates cell proliferation and apoptosis by regulating miR‐23a‐3p/SMC1A in acute myeloid leukemia.

The aim of this study was to determine the function of the NEAT1/miR‐23a‐3p/SMC1A axis in cell proliferation and apoptosis in acute myeloid leukemia (AML). Microarray analysis was used to screen differentially expressed lncRNAs/miRNAs/mRNAs in primary AML cells. The expression of nuclear paraspeckle assembly transcript 1 (NEAT1), miR‐23a‐3p, and structural maintenance of chromosome 1 alpha (SMC1A) in primary AML cells and THP‐1 cells were measured by quantitative real‐time polymerase chain reaction (qRT‐PCR). A Cell Counting Kit‐8 (CCK‐8) assay was used to analyze proliferation. Cell cycle progression and apoptosis were examined by flow cytometry. RNA immunoprecipitation (RIP) and dual‐luciferase assays were performed to determine the correlation between miR‐23a‐3p and NEAT1 or SMC1A. The qRT‐PCR illustrated that NEAT1 and SMC1A expression was decreased but that miR‐23a‐3p expression was increased in primary AML cells and THP‐1 cells compared with that in normal cells. The RIP assay and dual‐luciferase assay revealed the targeting relationship between miR‐23a‐3p and NEAT1 or SMC1A. The CCK‐8 assay showed that the overexpression of NEAT1 and SMC1A or repression of miR‐23a‐3p inhibited cell proliferation. Flow cytometry showed that the upregulation of NEAT1 and SMC1A or repression of miR‐23a‐3p promoted apoptosis and affected the cell cycle. NEAT1 repressed the expression of miR‐23a‐3p, and therefore promoted SMC1A, which in turn suppressed myeloid leukemia cell proliferation and enhanced apoptosis. 1.This study illustrates the molecular interaction between nuclear paraspeckle assembly transcript 1 (NEAT1), miR‐23a, and structural maintenance of chromosome 1 alpha (SMC1A) in acute myeloid leukemia (AML). 2.Reduced expression of NEAT1 induced the tumorigenesis and progression of AML through the miR‐23a‐3p/SMC1A axis. 3.These results suggest that this axis can be used as a promising therapeutic target to mitigate the progression of AML. [ABSTRACT FROM AUTHOR]