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MicroRNA-205-5p is upregulated in myelodysplastic syndromes and induces cell proliferation via PTEN suppression

Authors
Jang, Sook JinChoi, In-SunPark, GeonMoon, Dae-SooChoi, Ji-SeonNam, Myung-HyunYoon, Soo-YoungChoi, Cheol HeeKang, Seong-Ho
Issue Date
8월-2016
Publisher
PERGAMON-ELSEVIER SCIENCE LTD
Keywords
MDS; miR-205-5p; Upregulation; Diagnosis; Oncogenea
Citation
LEUKEMIA RESEARCH, v.47, pp.172 - 177
Indexed
SCIE
SCOPUS
Journal Title
LEUKEMIA RESEARCH
Volume
47
Start Page
172
End Page
177
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/87982
DOI
10.1016/j.leukres.2016.06.003
ISSN
0145-2126
Abstract
Micro (mi)RNA dysregulation is implicated in the development of myelodysplastic syndrome (MDS). Chromosomal abnormalities on 1q are frequently detected in Korean patients with MDS; however, how these are related to disease development is unknown. The present study compared the expression profiles of miRNAs encoded by chromosome 1q between 65 MDS patients and 11 controls. We found that miR-205-5p levels were 12.5 fold higher in the former (P=0.001). miR-205-5p level was increased in 44.7% of patients when an arbitrary 2(-Delta Ct) cut-off value of 1.25 was used. miR-205-5p expression data were used to generate a receiver operating characteristic (ROC) curve for miR-205-5p, for which the area under the curve (AUC) was 0.825 (95% confidence interval: 0.710-0.941; P=0.001). Moreover, transfection with a miR-205-5p mimic induced cell proliferation by inhibiting the expression of the tumor suppressor protein phosphatase and tensin homolog (PTEN). Our findings suggest that miR-205-5p upregulation contributes to MDS by suppressing PTEN and that miR-205-5p thus acts as an oncogene in hematopoietic cells. (C) 2016 Elsevier Ltd. All rights reserved.
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