up-regulation of mir-625-5p correlates with suppressed sox2, increased apoptosis, and cell cycle arrest via the pi3k/akt signalling pathway in acute myeloid leukaemia

Background: up-regulation of the microrna-625 and abnormal expression of the sox2 gene have been studied and seen in several tumors. few reports have also shown the aberrant expression of mir-625 and sox2 expression in various cancers. several studies have also confirmed that phosphatidylinositol 3' -kinase /protein kinase b pathways regulate hematological malignancies, including acute myeloid leukemia (aml). thus, this study aimed to investigate the effects of mir-625 up-regulation on proliferation, apoptosis, and cell cycle by targeting the sox2 gene via the downstream akt signaling pathway and cell cycle regulators, such as p21, p27, and cyclin e in the kg-1 cell line. materials and methods: cells obtained from the kg-1 cell line were cultured and transfected with plasmid dna (mir-625) and scrambled as the control using the lonza electroporation system. flow cytometry was used to evaluate cell cycle, proliferation, and apoptosis. relative gene expression was validated by qrt-pcr. all data were analyzed using graph pad prism 7.01 and rest 2009. results: kg-1 cells transfected with the mir625-gfp construct showed decreased proliferation, increased apoptosis, and induced cell cycle arrest. low levels of sox2, p21, cyclin e, and up-regulation of p27 were confirmed and validated by qrt-pcr ( p < 0.05 ). conclusion: mir-625 can be a promising approach to aid in the treatment of aml. however, further studies are required in this field.