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

• Published in: OncoTargets and therapy Vol. 12; pp. 2451 - 2463
• Main Authors: Yuan, Ye, Li, Shi-Lin, Cao, Yu-Lin, Li, Jun-Jun, Wang, Qiang-Ping
• Format: Journal Article
• Language: English
• Published: New Zealand Taylor & Francis Ltd 01.01.2019; Dove Medical Press
• Subjects: Apoptosis; Cancer therapies; Cell adhesion & migration; Cell cycle; Cell growth; Glioma; Immunoglobulins; Invasion; Kinases; Laboratories; LKB1; Lung cancer; Medical prognosis; Medical research; Metabolism; Original Research; Proteins; Snail; United States > US; China; NF-κB; snail; invasion; proliferation; migration; glioma; LKB1
• ISSN: 1178-6930; 1178-6930
• DOI: 10.2147/OTT.S193736

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. 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. 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. 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.