PT  - JOURNAL ARTICLE
AU  - YU-CHANG LIU
AU  - FEI-TING HSU
AU  - JING-GUNG CHUNG
AU  - MAO-CHI WENG
AU  - CHIEN-YI TING
AU  - CHIA-JUNG TSAI
AU  - ALEXANDER LAN
AU  - JENG-YUAN WU
AU  - CHARLES CHUNG-WEI LIN
AU  - SONG-SHEI LIN
TI  - Lenvatinib Induces AKT/NF-κB Inactivation, Apoptosis Signal Transduction and Growth Inhibition of Non-small Cell Lung Cancer <em>In Vivo</em>
AID  - 10.21873/anticanres.15068
DP  - 2021 Jun 01
TA  - Anticancer Research
PG  - 2867--2874
VI  - 41
IP  - 6
4099  - http://ar.iiarjournals.org/content/41/6/2867.short
4100  - http://ar.iiarjournals.org/content/41/6/2867.full
SO  - Anticancer Res2021 Jun 01; 41
AB  - Background/Aim: Non-small cell lung cancer (NSCLC) is the most common type of lung cancer with poor prognosis. Lenvatinib is a multi-kinase inhibitor that has the potential to suppress tumor progression. Our previous study suggested that lenvatinib induces cytotoxicity and apoptosis in CL-1-5-F4 cells in vitro. However, whether lenvatinib suppresses NSCLC progression in vivo remains unclear. Materials and Methods: Tumor growth inhibition and normal tissue toxicity evaluation following lenvatinib treatment were performed on CL-1-5-F4-bearing mice. Results: Tumor growth calculated by caliper and living cell intensity decreased by lenvatinib treatment as analysed by bioluminescence imaging. Phosphorylation of AKT, NF-κB, and NF-κB downstream proteins involved in tumor progression were reduced by lenvatinib in the tumor tissue. No pathological changes were found in the liver, kidney, and spleen after lenvatinib treatment. Conclusion: Induction of apoptosis and suppression of AKT/NF-κB were associated with lenvatinib-induced inhibition of the progression of NSCLC in vivo.