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miR-218 inhibits acute promyelocytic leukemia cell growth by targeting BMI-1. | LitMetric

miR-218 inhibits acute promyelocytic leukemia cell growth by targeting BMI-1.

Oncol Lett

Department of Hematology, Yuhuangding Hospital, Yantai, Shandong 264000, P.R. China.

Published: December 2017

AI Article Synopsis

  • Acute promyelocytic leukemia (APL) is a subtype of acute myelocytic leukemia, and the role of microRNA-218 (miR-218) in APL was investigated for its potential therapeutic benefits.
  • The study found that miR-218 is often downregulated in APL tissues and its overexpression can inhibit cell growth, cause cell cycle arrest, and trigger apoptosis in HL-60 cells.
  • It also revealed a negative relationship between miR-218 and BMI-1 expression, suggesting that targeting the miR-218/BMI-1 signaling pathway could provide new diagnostic and treatment strategies for APL.

Article Abstract

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 G/G 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5755149PMC
http://dx.doi.org/10.3892/ol.2017.7220DOI Listing

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