MicroRNA-616 promotes the growth and metastasis of non-small cell lung cancer by targeting SOX7 Retraction in /10.3892/or.2023.8623

Wang,Danping; Cao,Qifeng; Qu,Meijun; Xiao,Zhaoqun; Zhang,Minghui; Di,Songbo

doi:10.3892/or.2017.5854

MicroRNA-616 promotes the growth and metastasis of non-small cell lung cancer by targeting SOX7

Retraction in: /10.3892/or.2023.8623

Authors:
- Danping Wang
- Qifeng Cao
- Meijun Qu
- Zhaoqun Xiao
- Minghui Zhang
- Songbo Di
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Affiliations: Department of Respiratory Diseases, Chinese and Western Combined Hospital of Taizhou, Wenling, Zhejiang 317523, P.R. China, Department of Neurology, Chinese and Western Combined Hospital of Taizhou, Wenling, Zhejiang 317523, P.R. China
Published online on: July 28, 2017 https://doi.org/10.3892/or.2017.5854
Pages: 2078-2086
Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

MicroRNAs (miRNAs) are a group of important regulators in human types of cancer including non-small cell lung cancer (NSCLC). miR-616 has been found to be a novel cancer-related miRNA. However, the expression and biological function of miR-616 in NSCLC have not been investigated. In this study, qRT-PCR was performed to evaluate the level of miR-616 in NSCLC tissues. MTT, BrdU and Transwell assay were used to investigate the proliferation and metastasis ability of NSCLC cells. Subcutaneous injection model and tail vein injection model were used to evaluate the effect of miR-616 on the in vivo growth and metastasis of NSCLC cells. It was also found that the expression level of miR-616 was increased in NSCLC tissues and cell lines. Patients with a high level of miR-616 had a significantly shorter overall survival and disease-free survival. Functionally, miR-616 overexpression promoted while miR-616 knockdown inhibited the proliferation, migration and invasion of NSCLC cells. Moreover, miR-616 overexpression enhanced the subcutaneous growth and lung metastasis of NSCLC cells in nude mice. Mechanistically, SOX7 was confirmed to be the downstream target of miR-616 in NSCLC cells. Forced expression of SOX7 prevented the promoting effects of miR-616 overexpression on the proliferation and metastasis of NSCLC cells, while knockdown of SOX7 reversed the inhibitory effects of miR-616 knockdown on the proliferation and metastasis of NSCLC cells. In conclusion, the present study indicates that miR-616 is a promising biomarker and therapeutic target in NSCLC.

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