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

Haixia Li; Xuefei Tian; Paoqiu Wang; Jihong Hu; Rong Qin; Ronghua Xu; Kai Liu; Jingquan Hao; Nie Tian

doi:10.1080/15384047.2020.1740054

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

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

Authors

Haixia Li^{1

2}, Xuefei Tian³, Paoqiu Wang¹, Jihong Hu⁴, Rong Qin⁵, Ronghua Xu⁶, Kai Liu⁶, Jingquan Hao⁶, Nie Tian⁶

Affiliations

¹ The Third Department of Rehabilitation (Department of Integrated Chinese and Western Medicine), Hunan Children's Hospital , Changsha, Hunan, China.
² Hunan University of Chinese Medicine , Changsha, Hunan, China.
³ College of Integrated Chinese and Western Medicine, Hunan University of Chinese Medicine.
⁴ The First Department of Rehabilitation, Hunan Children's Hospital , Changsha, Hunan, China.
⁵ The Second Department of Rehabilitation, Hunan Children's Hospital , Changsha, Hunan, China.
⁶ Department of Hematology, The First Hospital of Hunan University of Traditional Chinese Medicine , Changsha, Hunan, China.

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.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Apoptosis / physiology
HEK293 Cells
HL-60 Cells
Humans
Leukemia, Myeloid, Acute / genetics*
Leukemia, Myeloid, Acute / metabolism
Leukemia, Myeloid, Acute / pathology
RNA, Long Noncoding / genetics*
RNA, Long Noncoding / metabolism
Receptors, Mineralocorticoid / genetics
Receptors, Mineralocorticoid / metabolism*
THP-1 Cells
Transfection
U937 Cells
Up-Regulation

Substances

NR3C2 protein, human
RNA, Long Noncoding
Receptors, Mineralocorticoid

Grants and funding

The 64th general project of China postdoctoral science foundation, No. 2018M642982; Major project of Hunan administration of traditional Chinese medicine, No. 201817.