Abnormal expression of microRNA-124 in patients with leukemia or myelodysplastic syndrome and its significance.
- Author:
Qiao XIA
1
;
Jun HU
;
Yue-Sheng MENG
Author Information
1. Department of Hematology, Shanghai East Hospital, Tongji University, Shanghai, China.
- Publication Type:Journal Article
- MeSH:
Adult;
Aged;
Aged, 80 and over;
Case-Control Studies;
DNA Methylation;
Female;
Humans;
Leukemia;
metabolism;
Male;
MicroRNAs;
genetics;
metabolism;
Middle Aged;
Myelodysplastic Syndromes;
metabolism;
Promoter Regions, Genetic;
Young Adult
- From:
Journal of Experimental Hematology
2012;20(2):358-361
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to investigate the abnormal expression of microRNA-124 (miR-124) in bone marrow cells of patients with leukemia or myelodysplastic syndrome (MDS) and its significance. The relative expression levels of miR-124 in bone marrow mononuclear cells from 33 patients with newly diagnosed leukemia or MDS, and 10 normal donors (as controls) were detected by stem-loop fluorescence real-time quantitative RT-PCR. The methylation levels of miR-124 promoter were detected by quantitative methylation specific PCR in partial MDS samples. The results indicated that as compared with normal control, lower levels of miR-124 (≤ 1/3) were found in 2/18 of leukemia patients and in 5/15 of MDS patients (among them ≤ 1/4 in 3/15 MDS patients). No statistically significance difference was observed between leukemia patients and normal controls (P = 0.725). However the difference was statistically significant between MDS group and control group (P = 0.031). Furthermore, an elevated methylation level of miR-124 promoter region in some of MDS patients (7/11) was detected by using quantitative methylation-specific PCR. The expression level of miR-124 was related with methylation level of promoter region (R(2) = 0.339, P = 0.018). It is concluded that the expression of miR-124 in partial MDS patients is inhibited, which may be associated with the abnormal methylation of its promoter.
