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

J Cell Physiol. 2019 May;234(5):6161-6172. doi: 10.1002/jcp.27393. Epub 2018 Sep 24.


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.

Keywords: NEAT1; SMC1A; acute myeloid leukemia; long noncoding RNA; miR-23a-3p.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / genetics
  • Cell Cycle Proteins / genetics*
  • Cell Proliferation / genetics
  • Chromosomal Proteins, Non-Histone / genetics*
  • Gene Expression Regulation, Leukemic / genetics*
  • Humans
  • Leukemia, Myeloid, Acute / genetics*
  • Leukemia, Myeloid, Acute / pathology
  • MicroRNAs / genetics*
  • RNA, Long Noncoding / genetics*
  • Tumor Cells, Cultured


  • Cell Cycle Proteins
  • Chromosomal Proteins, Non-Histone
  • MIRN23a microRNA, human
  • MicroRNAs
  • NEAT1 long non-coding RNA, human
  • RNA, Long Noncoding
  • structural maintenance of chromosome protein 1