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Original Research Article | OPEN ACCESS

MiR-26 targeting methyltetrahydrofolate reductase inhibits the proliferation of acute myeloid leukemia cells via JAK/STAT pathway

Yudi Miao1, Qiaojiajie Zhao2, Chengliang Li3

1Department of Hematology; 2Blood Research Department, Shaanxi Provincial people's Hospital, Xi’an; 3Department of General Practice, Guangzhou First People's Hospital, Guangzhou, China.

For correspondence:-  Chengliang Li   Email: lichengliang79@sina.com

Accepted: November 2022        Published: 29 December 2022

Citation: Miao Y, Zhao Q, Li C. MiR-26 targeting methyltetrahydrofolate reductase inhibits the proliferation of acute myeloid leukemia cells via JAK/STAT pathway. Trop J Pharm Res 2022; 21(12):2501-2506 doi: 10.4314/tjpr.v21i12.1

© 2022 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the effect of microribonucleic acid (miR)-26 targeting methyltetrahydrofolate reductase (MTHFR) on cell proliferation, cycle, and apoptosis in acute myeloid leukemia (AML).
Methods: The expressions of miR-26 in three types of human AML cell lines (HL-60, Kasumi-1, and KG-1a) and normal myeloid cell line (HS-5) were determined via quantitative reverse transcription-polymerase chain reaction (qRT-PCR), while the effect of the over-expression of miR-26 on the proliferation, cell cycle and apoptosis of AML cells was evaluated using cell counting kit-8 (CCK-8) assay and flow cytometry. The potential target for miR-26 was predicted using public miRNA database TargetScan, and whether miR-26 binds to the predicted target was determined using a dual-luciferase reporter assay. Western blotting was performed to determine the effect of miR-26 on Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway-associated proteins.
Results: expression level of miR-26 was significantly lower in all AML cell lines than in HS-5 cells (p < 0.05). Overexpression of miR-26 inhibited the proliferation of KG-1a cells, reduced the percentage of cells in S phase, increased those in G0/G1 phase, and enhanced apoptosis of KG-1a cells (p < 0.05). After overexpression of miR-26, protein expression levels of phosphorylated (p)-JAK and p-STAT were down-regulated, while those of JAK and STAT did not change significantly.
Conclusion: expression of miR-26 is down-regulated in AML, while MiR-26 targeting of MTHFR induces apoptosis and cycle arrest of AML cells through the JAK/STAT pathway, thus inhibiting AML cell proliferation in vitro.

Keywords: miRNA, Leukemia, Proliferation, Apoptosis

Impact Factor
Thompson Reuters (ISI): 0.523 (2021)
H-5 index (Google Scholar): 39 (2021)

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