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. 2020 Jul 2;21(7):615-622.
doi: 10.1080/15384047.2020.1740054. Epub 2020 Apr 26.

LINC01128 resisted acute myeloid leukemia through regulating miR-4260/NR3C2

Haixia Li  1   2 , Xuefei Tian  3 , Paoqiu Wang  1 , Jihong Hu  4 , Rong Qin  5 , Ronghua Xu  6 , Kai Liu  6 , Jingquan Hao  6 , Nie Tian  6
Affiliations

LINC01128 resisted acute myeloid leukemia through regulating miR-4260/NR3C2

Haixia Li et al. Cancer Biol Ther. .

Abstract

Acute myeloid leukemia (AML) is a prevalent class of blood disease with a high occurrence rate and relapse rate. The role of dysregulated microRNAs (miRNAs) in AML is emerging. MiR-4260 was identified to be a carcinogenic miRNA in colorectal cancer, but never has it been reported in AML. We aimed to study the function and mechanism of miR-4260 in AML. The miR-4260 level was higher in AML cell lines than the normal cell lines. Inhibition of miR-4260 hindered proliferation and increased apoptosis of AML cells. Mechanistically, long intergenic non-protein coding RNA 1128 (LINC01128) competed with nuclear receptor subfamily 3 group C member 2 (NR3C2) for miR-4260 so as to upregulate NR3C2. We identified the reduced levels of LINC01128 and NR3C2 in AML and it was suggested through rescue assays that LINC01128 repressed AML progression through regulating miR-4260/NR3C2 axis. In conclusion, we firstly uncovered that LINC01128 resisted acute myeloid leukemia through regulating miR-4260/NR3C2, providing novel clues for the treatment improvement of AML.

Keywords: AML; LINC01128; NR3C2; miR-4260.

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Figures

Figure 1.
Figure 1.
Expression and function of miR-4260 in AML.
Figure 2.
Figure 2.
LINC01128 could sponge miR-4260 in AML.
Figure 3.
Figure 3.
LINC01128 upregulated NR3C2 by targeting miR-4260 in AML.
Figure 4.
Figure 4.
Role of LINC01128/miR-4260/NR3C2 axis in AML.
See this image and copyright information in PMC

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