miR‑4306 inhibits the malignant behaviors of colorectal cancer by regulating lncRNA FoxD2‑AS1 Retraction in /10.3892/mmr.2024.13299

Ye,Jinjun; Liu,Jidong; Tang,Tao; Xin,Le; Bao,Xing; Yan,Yukuang

doi:10.3892/mmr.2021.12362

miR‑4306 inhibits the malignant behaviors of colorectal cancer by regulating lncRNA FoxD2‑AS1

Retraction in: /10.3892/mmr.2024.13299

Authors:
- Jinjun Ye
- Jidong Liu
- Tao Tang
- Le Xin
- Xing Bao
- Yukuang Yan
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Affiliations: Department of General Surgery, Shenzhen Longgang Central Hospital, Shenzhen, Guangdong 518116, P.R. China
Published online on: August 11, 2021 https://doi.org/10.3892/mmr.2021.12362
Article Number: 723
Copyright: © Ye et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

MicroRNA (miR)‑4306 and FoxD2‑adjacent opposite strand RNA 1 (FOXD2‑AS1) are cancer‑related genes involved in tumor progression. However, the potential functional roles of miR‑4306 and FoxD2‑AS1 in colorectal cancer (CRC) development remain unknown. The present study aimed to investigate the biological functions and the molecular mechanisms of miR‑4306 and FoxD2‑AS1 in CRC. Reverse transcription‑quantitative PCR analysis was performed to determine the expression levels of FoxD2‑AS1 and miR‑4306 in CRC tissues and cell lines. Functional experiments, including Cell Counting Kit‑8, colony formation, cell cycle assays and western blotting, were conducted to examine the effects of FoxD2‑AS1 and miR‑4306 on the malignant behaviors of CRC cells. In addition, the relationship between FoxD2‑AS1 and miR‑4306 was assessed using a dual‑luciferase reporter assay and Pearson's correlation analysis. Compared with normal samples and cells, FoxD2‑AS1 expression was increased and miR‑4306 expression was decreased in CRC tissues and cells. Functional experiments demonstrated that silencing FoxD2‑AS1 inhibited proliferation and induced cell arrest at G₀/G₁ phase in CRC cells, while the overexpression of FoxD2‑AS1 showed opposite results. Ki‑67 and proliferating cell nuclear antigen expression levels were decreased after transfection with small interfering RNA FoxD2‑AS1, but were increased after transfection with FoxD2‑AS1 overexpression plasmid. Furthermore, investigations into the underling mechanism revealed that FoxD2‑AS1 functioned as a molecular sponge of miR‑4306. The inhibitory effects of FoxD2‑AS1 silencing on CRC progression were reversed by miR‑4306 knockdown. Collectively, the present study demonstrated that FoxD2‑AS1 functioned as an oncogene in CRC progression, and that miR‑4306 could inhibit the malignant behaviors of CRC by regulating FoxD2‑AS1. Thus, the current study provided a promising therapeutic target for CRC treatment.

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