MicroRNA‑320a suppresses tumour cell proliferation and invasion of renal cancer cells by targeting FoxM1 Retraction in /10.3892/or.2024.8754

Zhao,Shiyue; Wang,Yangwei; Lou,Yan; Wang,Yonggang; Sun,Jing; Luo,Manyu; Li,Wen; Miao,Lining

doi:10.3892/or.2018.6597

MicroRNA‑320a suppresses tumour cell proliferation and invasion of renal cancer cells by targeting FoxM1

Retraction in 10.3892/or.2024.8754

Authors:
- Shiyue Zhao
- Yangwei Wang
- Yan Lou
- Yonggang Wang
- Jing Sun
- Manyu Luo
- Wen Li
- Lining Miao
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Affiliations: Department of Nephrology, The Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China, Department of Nephrology, The Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China, Department of Cardiology, The First Hospital of Jilin University, Changchun, Jilin 130041, P.R. China
Published online on: July 25, 2018 https://doi.org/10.3892/or.2018.6597
Pages: 1917-1926
Copyright: © Zhao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

An increasing body of evidence has indicated that microRNAs (miRNAs/miRs) may play an important role in tumourigenesis and tumour progression. Recent studies have demonstrated that miR‑320a is aberrantly expressed in a variety of different types of human cancer. The results of the present study confirmed that the expression of miR‑320a was decreased in clinical specimens and cell lines. Expression of miR‑320a inhibited the growth and invasive ability of ACHN and Caki‑1 cells. Bioinformatics analysis and a luciferase reporter assay demonstrated that forkhead box protein M1 (FoxM1) was directly regulated by miR‑320a. Rescue experiments in vitro revealed that the upregulation of FoxM1 antagonized the miR‑320a‑mediated malignant phenotype in renal cancer. Furthermore, experiments employing a xenograft mouse model revealed that the upregulation of miR‑320a inhibited the proliferation of renal cancer cells in nude mice when FoxM1 protein expression was reduced. Collectively, the present study demonstrated a novel molecular interaction regulated by miR‑320a, which may provide a novel insight into the treatments for renal cancer.

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