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Biomed Pharmacother. 2019 Apr;112:108623. doi: 10.1016/j.biopha.2019.108623. Epub 2019 Feb 20.

MiR-378 promoted cell proliferation and inhibited apoptosis by enhanced stem cell properties in chronic myeloid leukemia K562 cells.

Author information

1
Department of Central Lab, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China; The Key Lab of Precision Diagnosis and Treatment in Hematologic Malignancies of Zhenjiang City, China.
2
Department of Hematology, Kunshan Third People's Hospital, KunShan, Jiangsu, China.
3
Department of Central Lab, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China; The Key Lab of Precision Diagnosis and Treatment in Hematologic Malignancies of Zhenjiang City, China. Electronic address: qianjun0007@hotmail.com.
4
Department of Central Lab, Affiliated People's Hospital of Jiangsu University, Zhenjiang, Jiangsu, China; The Key Lab of Precision Diagnosis and Treatment in Hematologic Malignancies of Zhenjiang City, China. Electronic address: zqdeng2018@163.com.

Abstract

Dysregulation of miR-378 has been found in diverse types of tumors as well as in leukemia. The role of miR-378 in chronic myeloid leukemia (CML) remains unclear. The aim of the study was to reveal the potential effects of miR-378 in the pathological process and progress in CML. Our results showed general level of miR-378 was significant higher in CML patients compared to controls. Overexpression of miR-378 dramatically promoted cell proliferation and drug-resistance. Additionally, apoptosis was inhibited in cells transfected with miR-378. More and bigger stem cell sphere formation was observed in miR-378 transfected cells. Furthermore, enhanced expression of miR-378 was associated with upregulation of stem-cell makers OCT4 and c-Myc. Further study validated that miR-378 inhibited the expression of FUS1. Our research demonstrated the oncogenic nature of miR-378 in CML, and might contribute to the progress of CML.

KEYWORDS:

CML; K562 cell; MiR-378; Pluripotence

PMID:
30797151
DOI:
10.1016/j.biopha.2019.108623
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