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

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