INSR/AKT1 axis promotes cells proliferation and migration in acute myeloid leukemia.

Chemotherapy resistance represents a major challenge in relapsed and refractory acute myeloid leukemia (AML). Therefore, it is necessary to investigate the mechanisms underlying chemotherapy resistance in AML. INSR not only highly expressed in AML cells treated with chidamide, but also elevated in AML patients. Subsequent overexpression and knockdown experiments of INSR in AML cells demonstrated that INSR facilitates cell cycle transition from G1 to S phase and promotes AML cell proliferation. Furthermore, INSR upregulates vimentin and N-cadherin expression, thereby enhancing cell invasion and migration. By integrating transcriptome sequencing data with gene expression profile interactive analysis, we discovered that AKT1 expression levels were positively correlated with INSR expression, while AKT1 expression exhibited a negative correlation with the prognosis of AML patients. AKT1 expression inhibition reduced the proliferation and migratory activity of AML cells. Additionally, suppressing AKT1 expression diminished the impact of INSR on promoting AML cells proliferation, invasion, and migration. This study indicates that INSR expression is elevated in AML cells after treating with chidamide and that INSR promotes AML cells proliferation and migration by upregulating AKT1 expression.