LKB1 suppresses glioma cell invasion via NF-κB/Snail signaling repression
| Autor: | Ye Yuan, Yu-Lin Cao, Jun-Jun Li, Shi-Lin Li, Qiangping Wang |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
congenital hereditary and neonatal diseases and abnormalities Gene knockdown Kinase NF-κB Snail Biology medicine.disease 03 medical and health sciences chemistry.chemical_compound 030104 developmental biology 0302 clinical medicine Oncology chemistry Cell culture 030220 oncology & carcinogenesis Glioma biology.animal Cancer research medicine Pharmacology (medical) Signal transduction skin and connective tissue diseases Psychological repression |
| Zdroj: | OncoTargets and Therapy. 12:2451-2463 |
| ISSN: | 1178-6930 |
| DOI: | 10.2147/ott.s193736 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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