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MicroRNA-647 promotes the therapeutic effectiveness of argon–helium cryoablation and inhibits cell proliferation through targeting TRAF2 via the NF-κB signaling pathway in non-small cell lung cancer

Authors Zhang YS, Chen T, Cai YJ, Dong J, Bai F, Gao X, Tian L, Duan N, Liu D

Received 8 December 2017

Accepted for publication 6 April 2018

Published 10 October 2018 Volume 2018:11 Pages 6777—6784


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 3

Editor who approved publication: Dr XuYu Yang

Yun-song Zhang,1,* Tianzi Chen,1,* Ying Jiu Cai,1 Jianlin Dong,1 Fang Bai,1 Xiaojun Gao,1 Li Tian,2 Naiying Duan,2 Dan Liu3

1Department of Thoracic Surgery, Tianjin University of TCM Affiliated Wuqing Hospital of Traditional Chinese Medicine, Tianjin, People’s Republic of China; 2Department of Clinical Pharmacy, Tianjin Medical University, Tianjin, People’s Republic of China; 3Key Specialist Office, Tianjin University of TCM Affiliated Wuqing Hospital of Traditional Chinese Medicine, Tianjin, People’s Republic of China

*These authors contributed equally to this work

MicroRNA-647 (miR-647) has been reported to repress cell tumorigenic phenotype, while the function of miR-647 in non-small cell lung cancer was obscure.
Methods: The effect of miR-647 and TRAF2 on A549 and H1299 cells was explored through Methyl thiazolyl tetrazolium (MTT) assay, colony formation and cell cycle assays. Luciferase reporter assays, reverse transcription quantitative PCR (RT-qPCR) and Western blot assay were carried out to determine that TRAF2 is directly regulated by miR-647. The effect of miR-647/ TRAF2 axis on p65 protein level in nucleus or total was detected by Western blot assay.
Results: Here, we found that miR-647 was high expression in tumor that under argon-helium cryoablation treatment in contrast to the tumor under non argon-helium cryoablation treatment and inhibited cell proliferation of A549 and H1299 cells by inducing G1-S transition. TRAF2 was confirmed as a target of miR-647. TRAF2 overexpression partially rescued the suppressive function of miR-647 in A549 and H1299 cells. Moreover, we found that miR-647 repressed lung carcinogenesis by attenuating NF-κB pathway.
Conclusion: In all, our study demonstrates that miR-647 functions as tumor suppressor via targeting and down-regulating the expression of TRAF2 and NF-κB signaling pathway in non-small cell lung cancer.

Keywords: miRNA, miR-647, TRAF2, NF-κB, NSCLC, argon–helium cryoablation

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