Purpose: At present, there is a lack of precise knowledge on acute myeloid leukemia (AML) at the molecular level, and understanding its occurrence at the genetic level is conducive to the development of targeted therapies. Therefore, in this study the relationship between the lncRNA SNHG1 –miR183-5p–FOXO1 axis and AML was explored.
Methods: Expression of lncRNA SNHG16  and miR183-5p was quantified by quantitative real-time PCR, and the level of FOXO1 and other proteins was measured by Western blot. Expression vectors of lncRNA SNHG16 , miR183-5p, and FOXO1 were constructed to assess effects of the three on cell proliferation and apoptosis. MTT reduction assays were employed for cell proliferation, flow cytometry for cell cycle and apoptosis, and dual luciferase–reporter assays for the targeting relationship between lncRNA SNHG16  and miR183-5p and miR183-5p and FOXO1.
Results: lncRNA SNHG16  was highly expressed in peripheral blood/leukemia cell lines of patients with AML compared with normal human peripheral blood/peripheral blood mononuclear cells. miR183-5p was the target of lncRNA SNHG16  and FOXO1  the target gene of miR183-5p rather than lncRNA SNHG16. Absence of lncRNA SNHG16  led to upregulation of miR183-5p, promotion of apoptosis, and inhibition of proliferation. Suppression of miR183-5p accelerated cell proliferation and hindered apoptosis. miR183-5p negatively regulated FOXO1, and FOXO1 promoted proliferation and inhibited apoptosis. Inhibition of miR183-5p counteracted the changes caused by lncRNA SNHG16  absence.
Conclusion: lncRNA SNHG16  regulates the progress of AML via the miR183-5p–FOXO1 axis.
Keywords: acute myeloid leukemia, miR183-5p, lncRNA SNHG16 , FOXO1