Upregulation of AKAP12 by demethylation inhibits proliferation and increases chem osensitivity to adriamycin in leukemic cells

Purpose: To elucidate the role of AKAP12 in leukemia cells.Methods: Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting (WB) were employed to determine expression leukocyte cell lines, while 5-azacytidine was used treat cells, followed by assessment AKAP12. After constructing overexpressing vector pc-AKAP12 transfecting it into cells or treating with 5-azacytidine, counting kit-8 assay (CCK-8) proliferation. Cloning ability evaluated colony formation assay. Furthermore, flow cytometry measure degrees cycle apoptosis. The effect on PI3K/AKT determined western blot.Results: results showed that lowly expressed lymphocytic lines (p < 0.001), but reversed 5-azacytidine. Transfection treatment increased > inhibited proliferation clonality, arrested G1 phase as well induced In addition, signaling pathway AKAP12.Conclusion: is may also play a inhibiting progression suppressing activity pathway.Thus, targeting mght be potential strategy management lukemia.