miR-223 decreases cell proliferation and enhances cell apoptosis in acute myeloid leukemia via targeting FBXW7

Abstract

Abstract. The expression of microRNA-223 (miR-233) has been investigated in various types of cancer. However, to the best of our knowledge, the expression and function of miR-223 in acute myeloid leukemia (AML) remains to be elucidated. The expression of miR-223 was measured by reverse transcription-quantitative polymerase chain reaction. Following transfection with miR-223, cell viability assays, cell apoptosis assays, western blot analysis and luciferase assays were conducted in AML cell lines. In the present study, it was initially observed that miR-223 was downregulated in AML patients compared with healthy subjects. It was also demonstrated that miR-223 inhibited cell proliferation and enhanced cell apoptosis in AML cell lines. Additionally, the present study provided evidence that miR-223 may directly target F-box and WD repeat domain containing 7 in AML. The identification of candidate target genes of miR-223 may provide an understanding of the potential mechanisms underlying the development of AML. In conclusion, the results of the present study have therapeutic implications and may be exploited for further treatment of AML.

Low serum miR‐223 expression predicts poor outcome in patients with acute myeloid leukemia

“…Finally, miR‐223 was confirmed to be an independent prognostic factor for AML patients. Our findings were in line with previously published data, suggesting miR‐223 exerted a tumor suppressive function in AML . It was demonstrated that miR‐223 was downregulated in AML patients compared with healthy subjects.…”

“…It was demonstrated that miR‐223 was downregulated in AML patients compared with healthy subjects. Moreover, miR‐223 was shown to inhibit cell proliferation and enhance cell apoptosis in AML cell lines . Another research has also showed that there were significantly higher miR‐223 levels in patients with favorable prognosis, whereas patients with low miR‐223 expression levels were associated with worse outcome, by measuring miR‐223 expression in blasts from 115 AML patients.…”

“…miR-223 exerted a tumor suppressive function in AML. [16][17][18] It was demonstrated that miR-223 was downregulated in AML patients compared with healthy subjects. Moreover, miR-223 was shown to inhibit cell proliferation and enhance cell apoptosis in AML cell lines.…”

“…A study by Xiao et al revealed an inverse correlation between miR‐223 expression and FBXW7 expression. Elevated miR‐223 levels significantly inhibited cell motility and proliferation, as well as stimulated cell apoptosis in AML cell lines . Pulikkan et al reported miR‐223 levels were reduced in different AML subtypes, and ectopic miR‐223 expression suppressed tumorigenesis by regulating G1/S cell cycle phase transition by degrading E2F1 .…”

“…In the research of AML, upregulation of miR-155, 10 miR-210, 11 and miR-126-5p 12 was associated with poor clinical outcome of patients with AML, while high miR-370, 13 miR-328, 14 and miR-204 15 as well as stimulated cell apoptosis in AML cell lines. 16 Pulikkan et al reported miR-223 levels were reduced in different AML subtypes, and ectopic miR-223 expression suppressed tumorigenesis by regulating G1/S cell cycle phase transition by degrading E2F1. 17 In addition, Gentner and colleagues classified AML cases into four genetic risk groups and found patients with adverse prognosis exhibited lower miR-223 levels than those with favorable risk group.…”