MiR-181a Promotes Proliferation of Human Acute Myeloid Leukemia Cells by Targeting ATM.
- Author:
Jia-Ye HUA
1
;
Ying FENG
2
;
Ying PANG
2
;
Xu-Hong ZHOU
2
;
Bing XU
3
;
Mu-Xia YAN
4
Author Information
- Publication Type:Journal Article
- MeSH: Ataxia Telangiectasia Mutated Proteins; metabolism; Cell Proliferation; Down-Regulation; HL-60 Cells; Humans; Leukemia, Myeloid, Acute; metabolism; pathology; MicroRNAs; genetics; metabolism; Transfection
- From: Journal of Experimental Hematology 2016;24(2):347-351
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate miR-181a function and regulation mechanism by identifying miR-181a target genes in acute myeloid leukemia (AML).
METHODSThe HL-60 cells of human AML was transfected by small molecular analog miR-181a, the cell proliferation was detected by CCK-8 method after electroporation in HL-60 cell lines. Target genes of miR-181a were predicted and analyzed by the bioinformatics software and database. Target genes were confirmed by HL-60 cell line and the patient leukemia cells.
RESULTSOverexpressed miR-181a in HL-60 cell line significantly enhanced cell proliferation compared with that in control (P < 0.05). Dual luciferase reporter gene assay showed that miR-181a significantly suppressed the reporter gene activity containing ATM 3'-UTR by about 56.8% (P < 0.05), but it didn't suppress the reporter gene activity containing 3'-UTR ATM mutation. Western blot showed that miR-181a significantly downregulated the expression of ATM in human leukemia cells. It is also found that miR-181a was significantly increased in AML, which showed a negative correlation with ATM expression.
CONCLUSIONmiR-181a promotes cell proliferation in AML by regulating the tumor suppressor ATM, thus it plays the role as oncogene in pathogenesis of AML.
