Abstract: Objective To investigate the effect of long non-coding RNA (lncRNA) SNHG7 on cell drug resistance through inhibiting microRNA-186(miR-186). Methods Peripheral blood was taken from newly diagnosed AML patients, recurrent/refractory AML patients and healthy controls. AML adriamycin sensitive cells (HL60) and AML adriamycin resistant cells (HL60/ADM) were used to detect the expression of SNHG7 and miR-186 in peripheral blood and cell samples by fluorescence quantitative PCR. The sensitivity of HL60 and HL60/ADM cells to adriamycin was determined by CCK8 assay and the 50% inhibitory concentration(IC₅₀) was calculated. Sh-SNHG7 or miR-186 mimic or miR-186 inhibitor was transfected into HL60/ADM cells. The expres- sion of SNHG7 and miR-186 was detected by fluorescence quantitative PCR, the dose response and IC₅₀ of HL60/ADM to adriamycin were detected by CCK8. Double luciferase reporter gene assay was used to detect the targeted binding of SNHG7 to miR-186. Results The expression of SNHG7 in the serum of newly diagnosed AML and recurrent/refractory AML patients was significantly higher than that of normal controls, and the trend of miR-186 was contrary to that of SNHG7 (P＜0.01). Compared with HL60 cells, HL60/ADM cells were treated with adriamycin at different concentrations, and the IC₅₀ value of adriamycin on HL60/ADM (3.36±0.65) cells was significantly higher than that of HL60 cells (0.43±0.16) (P＜0.001). SNHG7 expression was significantly higher(P＜0.05) in HL60/ADM cells and miR-186 was significantly lower (P＜0.05). Transfection with sh-SNHG7 or miR-186 mimic in HL60/ADM cells increased the sensitivity to adriamycin and decreased the IC₅₀ value from 3.17±0.61 to 2.30±0.31 and 3.22±0.62 to 2.16±0.33, respectively (P＜0.05). Dual-luciferase reporter assay confirmed that SNHG7 could bind miR-186. Conclusions SNHG7 enhances drug resistance of AML cells during chemotherapy through inhibition of miR-186.

Key words: SNHG7, miR-186, proliferation, drug-resistance, acute myeloid leukemia