Basic & Clinical Medicine ›› 2021, Vol. 41 ›› Issue (2): 171-177.

• Original Articles • Previous Articles     Next Articles

LncRNA SNHG7 enhances the drug resistance of human acute myeloid leukemia cells through inhibiting miR-186

ZHU Juan1, ZHOU Ying2, LI Ying-jia1*   

  1. 1. Department of Laboratory Medicine, the Third Xiangya Hospital of Central South University, Changsha 410013;
    2. Department of Clinical Laboratory,Changsha Central Hospital,Changsha 410004, China
  • Received:2020-05-06 Revised:2020-10-13 Online:2021-02-05 Published:2021-01-19
  • Contact: *

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

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