TY - JOUR T1 - Lenvatinib Inhibits AKT/NF-κB Signaling and Induces Apoptosis Through Extrinsic/Intrinsic Pathways in Non-small Cell Lung Cancer JF - Anticancer Research JO - Anticancer Res SP - 123 LP - 130 DO - 10.21873/anticanres.14757 VL - 41 IS - 1 AU - YU-CHANG LIU AU - BO-HAN HUANG AU - JING-GUNG CHUNG AU - WEI-LIN LIU AU - FEI-TING HSU AU - SONG-SHEI LIN Y1 - 2021/01/01 UR - http://ar.iiarjournals.org/content/41/1/123.abstract N2 - 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. ER -