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LKB1 suppresses glioma cell invasion via NF-κB/Snail signaling repression

Authors Yuan Y, Li SL, Cao YL, Li JJ, Wang QP

Received 7 November 2018

Accepted for publication 4 February 2019

Published 2 April 2019 Volume 2019:12 Pages 2451—2463

DOI https://doi.org/10.2147/OTT.S193736

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Cristina Weinberg

Peer reviewer comments 3

Editor who approved publication: Dr Sanjeev Srivastava


Ye Yuan,1 Shi-Lin Li,2 Yu-Lin Cao,3 Jun-Jun Li,1 Qiang-Ping Wang1

1Department of Neurosurgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, People’s Republic of China; 2Department of Neurology, Qitaihe Qimei Hospital, Qitaihe 154600, People’s Republic of China; 3Department of Hematology, Wuhan General Hospital of Guangzhou Military Area Command, Wuhan 430070, People’s Republic of China

Background: Liver kinase B1 (LKB1) is involved in various human diseases. Aberrant expression of LKB1 expression is involved in glioma progression and associated with prognosis, however, the specific mechanism involving NF-κB/Snail signaling pathways remain unknown.
Materials and methods: In the present study, quantitative real-time PCR analysis was used to investigate the expression of LKB1 tumor tissue samples and cell lines. In glioma cell lines, CCK-8 assay, transwell invasion and migration assays were used to investigate the effects of LKB1on proliferation and invasion.
Results: We observed that LKB1 knockdown promoted glioma cell proliferation, migration and invasion. This effect was induced through NF-κB/Snail signaling activation. Also, LKB1 overexpression suppressed proliferation, migration, and invasion, which could be rescued by Snail overexpression.
Conclusion: Taken together, our results show that LKB1 knockdown promotes remarkably glioma cell proliferation, migration and invasion by regulating Snail protein expression through activating the NF-κB signaling. This may serve as a potential prognostic marker and therapeutic target for glioma.

Keywords: glioma, proliferation, migration, invasion, LKB1, NF-κB, snail

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