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miR-130a-Mediated KLF3 Can Inhibit the Growth of Lung Cancer Cells

Authors Wei MC, Wang YM, Wang DW

Received 26 October 2020

Accepted for publication 8 March 2021

Published 6 April 2021 Volume 2021:13 Pages 2995—3004

DOI https://doi.org/10.2147/CMAR.S281203

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 5

Editor who approved publication: Dr Eileen O'Reilly


Ming-Chao Wei,1 Yu-Min Wang,2 Da-Wei Wang3

1Department of Thoracic Surgery, Yantai Affiliated Hospital of Binzhou Medical University, Shandong, People’s Republic of China; 2Binzhou Medical University, Shandong, People’s Republic of China; 3Department of Thoracic Surgery, Yantai Mountain Hospital, Shandong, People’s Republic of China

Correspondence: Da-Wei Wang
Department of Thoracic Surgery, Yantai Mountain Hospital, Yantai, Shandong, 264001, People’s Republic of China
Tel +86-0535-6602183
Email [email protected]

Background: The role of microRNA (miR) in tumors has been reported in numerous articles. Previous studies have found that miR-130a is low expressed in lung cancer, but the related mechanism has not been fully elucidated. This study mainly explores the mechanism of miR-130a in lung cancer, so as to provide potential therapeutic targets for clinical applications.
Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-130a and KLF3 in the tissues of lung cancer patients. The miR-130a-mimics and miR-130a-inhibit were constructed. Cell proliferation, invasion, migration and apoptosis were determined by CCK-8, transwell, scratch test and flow cytometry. Western Blot was used to determine the expression of KLF3 protein in cells, and the dual-luciferase reporter to determine the relationship between KLF3 and miR-130a.
Results: miR-130a shows low expression in NSCLC patients, while KLF3 shows high expression, exhibiting a negative correlation. The 5-year survival rate of patients with low miR-130a expression and high KLF3 expression was reduced. Cox regression analysis showed that miR-130a was an independent prognostic factor for NSCLC patients. The dual-luciferase reporter revealed that miR-130a bound to KLF3 in a targeted manner, and cell experiments showed that miR-130a could inhibit the growth of lung cancer cells by regulating the expression of KLF3.
Conclusion: miR-130a shows low expression in lung cancer and predicts a poor prognosis. In addition, up-regulation of miR-130a can down-regulate KLF3 and inhibit the growth of lung cancer.

Keywords: miR-130a, KLF3, lung cancer, prognosis

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