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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
Source :
OncoTargets and Therapy, Vol Volume 12, Pp 2451-2463 (2019)
Publication Year :
2019
Publisher :
Dove Medical Press, 2019.

Abstract

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

Details

Language :
English
ISSN :
11786930
Database :
OpenAIRE
Journal :
OncoTargets and Therapy
Accession number :
edsair.doajarticles..204d639ed7f353d74fdf539393884b39