miR‑218 inhibits acute promyelocytic leukemia cell growth by targeting BMI‑1
- Yan Wang
- Hai‑Hong Sun
- Ming‑Hua Sui
- Jun‑Jie Ma
Published online on: October 19, 2017
Acute promyelocytic leukemia (APL) is a subtype of acute myelocytic leukemia. Previous studies have reported a number of functions and therapeutic roles of microRNAs (miRs) in APL, and have suggested that miR‑218 acts as a tumor suppressor in a number of types of human cancer; however, its role in APL remains unclear. In the present study, the expression of miR‑218 and its effects on the viability and proliferation of HL‑60 cells was investigated. Reverse transcription‑quantitative polymerase chain reaction analysis demonstrated that miR‑218 was frequently downregulated in APL marrow tissues compared with normal marrow tissues. Overexpression of miR‑218 significantly inhibited cell proliferation, arrested the cell cycle in the G0/G1 phase and induced apoptosis. In addition, B‑cell‑specific Moloney murine leukemia virus integration site 1 (BMI‑1) mRNA expression was negatively associated with miR‑218 expression; BMI‑1 mRNA and protein expression were downregulated following transfection with miR‑218 mimic. These results indicate that miR‑218 functions as tumor suppressor in APL, and the miR‑218/BMI‑1 signaling axis may be a potential novel diagnostic marker and therapeutic target for the treatment of APL.