PTEN/AKT signaling mediates chemoresistance in refractory acute myeloid leukemia through enhanced glycolysis.

PTEN/AKT signaling mediates chemoresistance in refractory acute myeloid leukemia through enhanced glycolysis. Oncol Rep. 2019 Sep 12;: Authors: Ryu MJ, Han J, Kim SJ, Lee MJ, Ju X, Lee YL, Son JH, Cui J, Jang Y, Chung W, Song IC, Kweon GR, Heo JY Abstract Primary refractory acute myeloid leukemia (AML) and early recurrence of leukemic cells are among the most difficult hurdles to overcome in the treatment of AML. Moreover, uncertainties surrounding the molecular mechanism underlying refractory AML pose a challenge when it comes to developing novel therapeutic drugs. However, accumulating evidence suggests a contribution of phosphatase and tensin homolog (PTEN)/protein kinase B (AKT) signaling to the development of refractory AML. To assess PTEN/AKT signaling in AML, two types of AML cell lines were evaluated, namely control HL60 cells and KG1α cells, a refractory AML cell line that is resistant to idarubicin and cytarabine (AraC) treatment. Changes in the expression level of glycolysis‑ and mitochondrial oxidative phosphorylation‑related genes and proteins were evaluated by reverse transcription‑quantitative polymerase chain reaction and western blot analyses, respectively. The mitochondrial oxygen consumption and extracellular acidification rates were measured using an XF24 analyzer. CCK8 assay and Annexin V/PI staining were used to analyze cell viability and cellular apoptosis, respectively. The PTEN protein was found to be ...
Source: Oncology Reports - Category: Cancer & Oncology Tags: Oncol Rep Source Type: research