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miR-331-3p Inhibits Tumor Cell Proliferation, Metastasis, Invasion by Targeting MLLT10 in Non-Small Cell Lung Cancer

Authors Tian QQ, Xia J, Zhang X, Gao BQ, Wang W

Received 13 February 2020

Accepted for publication 24 June 2020

Published 14 July 2020 Volume 2020:12 Pages 5749—5758

DOI https://doi.org/10.2147/CMAR.S249686

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Sanjeev Srivastava


Qing-Qing Tian,1 Jing Xia,2 Xin Zhang,3 Bao-Qin Gao,4 Wei Wang5

1Department of Pathology, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China; 2General Department of Houhu, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China; 3Department of Radiology, The Fourth People’s Hospital of Huai’an, Huai’an, Huai’an, People’s Republic of China; 4Operating Room, Huai’an Second People’s Hospital and the Affiliated Huai’an Hospital of Xuzhou Medical University, Huai’an, People’s Republic of China; 5Department of Oncology, Huai’an Second People’s Hospital and the Affiliated Huai’an Hospital of Xuzhou Medical University, Huai’an, People’s Republic of China

Correspondence: Bao-Qin Gao
Operating Room, Huai’an Second People’s Hospital and the Affiliated Huai’an Hospital of Xuzhou Medical University, Huai’an, People’s Republic of China
Email hagbqsyh@163.com
Wei Wang
Department of Oncology, Huai’an Second People’s Hospital and the Affiliated Huai’an Hospital of Xuzhou Medical University, Huai’an, People’s Republic of China
Email Wwei2003@126.com

Objective: Mounting research has established the role of microRNAs (miRNAs) as oncogenes or anti-oncogenes (tumor suppressors) in the development and progression of several cancers. The purpose of our current study is to delineate the roles and functional mechanisms of miR-331-3p and MLLT10 in non-small cell lung cancer (NSCLC) tumorigenesis.
Patients and Methods: Quantitative reverse transcription-polymerase chain reaction (RT-qPCR) was employed to measure miR-331-3p expression levels in twenty-six matched tumor tissues and non-cancerous tissues collected from patients suffering from NSCLC, and from six NSCLC cell lines separately: A549, H1650, H292, H1299, H1944 and BEAS-2b. We employed the dual-luciferase activity assay to check whether the putative gene, MLLT10, was a downstream target of miR-331-3p in NSCLC pathogenesis and development. Western blot was conducted to analyze the protein expression levels of MLLT10 (AF10), E-cadherin, Vimentin, and GAPDH. CCK-8 assay, transwell migration assay, and transwell invasion assay were carried out to observe the functions of miR-331-3p and MLLT10 on NSCLC tumor cell proliferation, metastasis, and invasion, respectively. To identify whether the metastasis of NSCLC tumor cells was EMT-mediated, supplementary experiments involving E-cadherin and Vimentin were implemented.
Results: miR-331-3p was downregulated in NSCLC, which promoted tumor cell proliferation, whereas the overexpression of miR-331-3p inhibited tumor cell proliferation. Being a direct target of miR-331-3p, MLLT10 was negatively modulated by miR-331-3p, which suppressed tumor cell proliferation, migration, and invasion in NSCLC. However, MLLT10 overexpression alleviated the above inhibitory effects. Furthermore, EMT-mediated metastasis was proved to be present in NSCLC.
Conclusion: miR-331-3p played a suppressor role in NSCLC tumor cell proliferation, EMT-mediated metastasis, and invasion by targeting MLLT10. Our findings highlighted that miR-331-3p/MLLT10 axis could be useful as a clinical diagnostic marker and therapeutic target in NSCLC patients.

Keywords: NSCLC, miR-331-3p, MLLT10, EMT-mediated metastasis

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