Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

MiR-598-3p functions as a tumor suppressor in pediatric T-cell acute lymphoblastic leukemia

Zhang Qiang¹, Jinhua Feng¹, Chunlian Wang², Meizhu Zheng³, Zhuoyu Wen⁴

¹Department of Pediatrics, Changchun University of Traditional Chinese Medicine Affiliated Hospital, Changchun; ²Department of Pediatrics, Jilin College of Traditional Chinese Medicine, Changchun, Jilin Province; ³Department of Child Healthcare, Jilin Women and Children Health Hospital, Changchun, Jilin Province, 130021; ⁴Department of Pediatrics, Northwest Women and Children's Hospital, Xi'an, Shaanxi Province 710054, China.

For correspondence:- Zhuoyu Wen Email: wenzhuoyu0813@163.com Tel:+862989122753

Accepted: 20 February 2021 Published: 31 March 2021

Citation: Qiang Z, Feng J, Wang C, Zheng M, Wen Z. MiR-598-3p functions as a tumor suppressor in pediatric T-cell acute lymphoblastic leukemia. Trop J Pharm Res 2021; 20(3):497-503 doi: 10.4314/tjpr.v20i3.8

© 2021 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 role of miR-598-3p in pediatric T-cell acute lymphoblastic leukemia (T-ALL).

Methods: The expression of miR-598-3p in mononuclear cells isolated from the peripheral blood samples of children with or without T-ALL was assessed using real-time quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Cell viability or proliferation of T-ALL cell lines was evaluated using cell counting kit-8 assay or bromodeoxyuridine staining, respectively. The target gene of miR-598-3p was predicted and validated using luciferase reporter assay, while the underlying mechanism involved in miR-598-3p-mediated T-ALL was determined by western blot analysis.

Results: MiR-598-3p was reduced in the peripheral blood mononuclear cells of T-ALL patients. Ectopic miR-598-3p expression decreased T-ALL cell viability and suppressed proliferation, while miR-598-3p interference showed reversed effects. Additionally, the target gene of miR-598-3p, Dishevelled, EGL-10, and Pleckstrin domain-containing mTOR-interacting protein (DEPTOR), was down-regulated by miR-598-3p in T-ALL. MiR-598-3p decreased phospho (p)-AKT protein expression, while AKT inhibition counteracted the suppressive effects of miR-598-3p silencing on T-ALL cell viability and proliferation.

Conclusion: MiR-598-3p/DEPTOR is involved in the proliferation of T-ALL through AKT pathway, thus providing a potential novel application in pediatric T-ALL.

Keywords: MiR-598-3p, DEPTOR, Progression, AKT pathway, Pediatric T-ALL