PT  - JOURNAL ARTICLE
AU  - YU-CHANG LIU
AU  - BO-HAN HUANG
AU  - JING-GUNG CHUNG
AU  - WEI-LIN LIU
AU  - FEI-TING HSU
AU  - SONG-SHEI LIN
TI  - Lenvatinib Inhibits AKT/NF-κB Signaling and Induces Apoptosis Through Extrinsic/Intrinsic Pathways in Non-small Cell Lung Cancer
AID  - 10.21873/anticanres.14757
DP  - 2021 Jan 01
TA  - Anticancer Research
PG  - 123--130
VI  - 41
IP  - 1
4099  - http://ar.iiarjournals.org/content/41/1/123.short
4100  - http://ar.iiarjournals.org/content/41/1/123.full
SO  - Anticancer Res2021 Jan 01; 41
AB  - Background/Aim: Non-small cell lung cancer (NSCLC) is a serious disease and the leading cause of death globally. Overexpression of protein kinase B/nuclear factor-kappa B (NF-κB) signaling transduction of NSCLC cells was recognized as a potential therapeutic target. Lenvatinib is a multiple kinase inhibitor against vascular endothelial growth factor receptor family. However, whether lenvatinib may affect AKT/NF-κB in NSCLC remains unknown. Materials and Methods: MTT assay, NF-κB reporter gene assay, flow cytometry, tranwell migration/invasion analysis and western blotting were used to identify the alteration of cell viability, NF-κB activation, apoptosis effect, migration/invasion potential and AKT/NF-κB related protein expression, respectively, in CL-1-5-F4 cells after lenvatinib treatment. Results: The cell viability and NF-κB activity were suppressed by lenvatinib. Extrinsic and intrinsic apoptosis were activated by lenvatinib. Additionally, the metastatic potential of CL-1-5-F4 cells was also suppressed by lenvatinib. Conclusion: Altogether, lenvatinib induced extrinsic/intrinsic apoptosis and suppressed migration/invasion ability of NSCLC cells that was associated with AKT/NF-κB signaling inactivation.