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MiR-1299 Impedes the Progression of Non-Small-Cell Lung Cancer Through EGFR/PI3K/AKT Signaling Pathway

Authors Cao S, Li L, Li J, Zhao H

Received 18 February 2020

Accepted for publication 8 July 2020

Published 30 July 2020 Volume 2020:13 Pages 7493—7502

DOI https://doi.org/10.2147/OTT.S250396

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Editor who approved publication: Dr Federico Perche


Shengya Cao,1,* Longfei Li,2,* Jia Li,3 Hongying Zhao4

1Department of Clinical Laboratory, Xuzhou Cancer Hospital, Xuzhou, Jiangsu, People’s Republic of China; 2Department of Thoracic Surgery, Xuzhou Cancer Hospital, Xuzhou, Jiangsu, People’s Republic of China; 3Department of Central Laboratory, Xuzhou Cancer Hospital, Xuzhou, Jiangsu, People’s Republic of China; 4Department of Oncology, Xuzhou Cancer Hospital, Xuzhou, Jiangsu, People’s Republic of China

*These authors contributed equally to this work

Correspondence: Hongying Zhao
Department of Oncology, Xuzhou Cancer Hospital, Xuzhou, Jiangsu, People’s Republic of China
Email dqlnyyzhao@126.com

Background: Non-small-cell lung cancer (NSCLC) is one of the most malignant tumors. In which, numerous miRNAs had been reported to participate in the pathogenesis. However, the expression and function of miR-1299 in NSCLC are not clear.
Methods: To explore the roles of miR-1299 in NSCLC, we detected the levels of miR-1299 in clinical samples of NSCLC and investigated the role of miR-1299 in the regulation of the NSCLC cells proliferation, metastasis, and EMT. Luciferase reporter assay was employed to verify the target of miR-1299. Additionally, the proliferation, metastasis, and EMT of A549 and H1299 cells were analyzed after the overexpression and knockdown of miR-1299.
Results: We found that the miR-1299 expression negatively corresponded with the clinical stage and overall survival in NSCLC patients. Overexpression of miR-1299 inhibited the migration, invasion, and EMT of A549 and H1975 cells. Meanwhile, we proved that miR-1299 is the sponge of EGFR. Besides, our results suggested that miR-1299 inhibits the progression of NSCLC cells through the PI3K/Akt signal pathway.
Conclusion: We demonstrated that miR-1299 inhibits the progression of NSCLC through the EGFR/PI3K/Akt signal pathway. Therapeutic intervention targeting the miR-1299 may provide a potential strategy for the treatment of NSCLC.

Keywords: miR-1299, NSCLC, EGFR, PI3K/Akt

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