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Original Research Article | OPEN ACCESS

KLF8 enhances acute myeloid leukemia cell growth and glycolysis via AKT/mTOR pathway

Tingting Lu1, Qiurong Zhang1, Xiao Wu1, Senjun Liu2

1Department of Hematology, Zhangjiagang First People's Hospital, Suzhou, Jiangsu Province 215600, China; 2Department of Hematology, Lishui City People's Hospital, Lishui, Zhejiang Province 323000, China.

For correspondence:-  Senjun Liu   Email: Liusenjun_666@163.com   Tel:+865782780108

Accepted: 30 May 2022        Published: 30 June 2022

Citation: Lu T, Zhang Q, Wu X, Liu S. KLF8 enhances acute myeloid leukemia cell growth and glycolysis via AKT/mTOR pathway. Trop J Pharm Res 2022; 21(6):1169-1175 doi: 10.4314/tjpr.v21i6.5

© 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 determine the role and mechanisms of Krüppel-like transcription factor 8 (KLF8) in acute myeloid leukemia (AML).
Methods: The transcriptional and translational levels of KLF8 in AML cell lines were determined by quantitative real time-polymerase chain reaction (qRT-PCR) and western blotting. Two RNAs targeting KLF8 were transfected into KG-1 and HL-60 cells. The growth and apoptosis of AML cells were determined using CCK-8, 5-ethynyl-2-deoxyuridine (EdU), flow cytometry, and western blot assays. Glycolysis was evaluated by relative glucose consumption, lactate generation, ATP levels, and hexokinase II (HK2), while glucose transporter 1 (GLUT1) protein expression levels. AKT, phosphorylated AKT (p-AKT), mammalian target of rapamycin (mTOR), and p-mTOR expression levels were assessed by western blot.
Results: KLF8 mRNA and protein expression levels were elevated in AML cells (p < 0.01). KLF8 knockdown in AML cells decreased cell viability, EdU-positivity, relative glucose consumption, lactate generation, ATP levels, and HK2 and GLUT1 protein levels (p < 0.01). Apoptosis increased in KG-1 and HL-60 cells, with enhanced Bax and reduced Bcl-2 protein levels, after transfection with sh-KLF8. The relative expression levels of p-AKT/AKT and p-mTOR/mTOR were reduced in KG-1 and HL-60 cells transfected with sh-KLF8.
Conclusion: Downregulation of KLF8 inhibits proliferation and glycolysis, and also promotes apoptosis in AML cells via AKT/mTOR pathway.

Keywords: Acute myeloid leukemia, KLF8, Proliferation, Apoptosis, Glycolysis, AKT/mTOR

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

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