MicroRNA‑139‑5p inhibits cell viability, migration and invasion and suppresses tumor growth by targeting HDGF in non‑small cell lung cancer Retraction in /10.3892/ol.2023.14090

Zhang,Zuxiong; Li,Weizhi; Jiang,Damei; Liu,Chi; Lai,Zhenghong

doi:10.3892/ol.2020.11296

MicroRNA‑139‑5p inhibits cell viability, migration and invasion and suppresses tumor growth by targeting HDGF in non‑small cell lung cancer

Retraction in: /10.3892/ol.2023.14090

Authors:
- Zuxiong Zhang
- Weizhi Li
- Damei Jiang
- Chi Liu
- Zhenghong Lai
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Affiliations: Department of Cardiothoracic Surgery, First Affiliated Hospital of Gannan Medical University, Ganzhou, Jiangxi 341000, P.R. China, Department of Radiotherapy, Tumor Hospital of Ganzhou, Ganzhou, Jiangxi 341000, P.R. China, Department of Obstetrics and Gynecology, Ganzhou Municipal Hospital, Ganzhou, Jiangxi 341000, P.R. China, School of Medical and Life Sciences, Chengdu University of TCM, Chengdu, Sichuan 610072, P.R. China
Published online on: January 13, 2020 https://doi.org/10.3892/ol.2020.11296
Pages: 1806-1814
Copyright : © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY 4.0].

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Abstract

MicroRNA (miRNAs) serve key roles in the progress of various types of cancer. The expression of miRNA (miR)‑139‑5p is downregulated in several types of tumor and has been recognized as a tumor suppressor. However, the role of miR‑139‑5p in non‑small cell lung cancer (NSCLC) has not been investigated in detail. In the present study, it was demonstrated that miR‑139‑5p was significantly downregulated in NSCLC cells and tissues, and the overexpression of miR‑139‑5p in vitro induced apoptosis and significantly inhibited the viability and proliferation of A549 and H1299 cells. In addition, upregulation of miR‑139‑5p significantly inhibited the migration and invasion of A549 and H1299 cells. Hepatoma‑derived growth factor (HDGF) was identified as a direct target of miR‑139‑5p. Rescue experiments demonstrated that the inhibitory function of miR‑139‑5p on cell viability, migration and invasion was partially mediated by suppressing HDGF expression. Furthermore, miR‑139‑5p exhibited efficient inhibition of tumor growth in a xenograft tumor mouse model of A549 cells. In summary, the results from the present study suggested that miR‑139‑5p may serve an important role in NSCLC by targeting HDGF and causing inhibition of cell viability and metastasis, as well as induction of apoptosis. miR‑139‑5p may also have the potential to serve as a therapeutic target for the treatment of NSCLC.

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