miR-22/TET2/p53-Feedback Loop Regulates Cell Proliferation and Apoptosis of k562 cells

Abstract

BackgroundChronic myeloid leukemia (CML) is a major global health threat due to its low cure rate and high fatality rate. Studies have reported that miR-22, TET2, and p53 play a vital role in the progression of leukemia. However, it is unclear whether there is feedback regulation between them.MethodsTransfection efficiency of miR-22 and TET2 was detected by qRT-PCR. CCK-8 assay was applied to measure the proliferation ability of K562 cells. Flow cytometry was used for evaluation the cell cycle and apoptosis rate of K562 cells after transfection. Moreover, the interaction between miR-22, TET2 and P53 was analyzed by luciferase reporter gene assay.ResultsExperiments indicated that the TET2 expression was decreased and apoptosis was increased in the miR-22 mimic group, and cell cycle was arrested in G0/G1phase, the proliferation was markedly inhibited. Meanwhile we found that TET2 can affect the expression of p53. Then, we directly proved p53 inhibition miR-22 transcription, whereas miR-22 as a transcriptional repressor, TET2 expression is negatively regulated to form a feedback loop.ConclusionsmiR-22, TET2 and p53 can form a feedback loop and thus affect cell proliferation and apoptosis of chronic myeloid leukemia cells.