Inhibition of JNK/STAT3/NF-KB pathway-mediated migration and clonal formation of lung adenocarcinoma A549 cells by daphnetin

• Published in: Cell adhesion & migration 2024-12, Vol.18 (1), p.27-37
• Main Authors: Lv, Zhe, Du, Yuna, Zhang, Huiqing, Fang, Hui, Guo, Yujie, Zeng, Lifeng, Chen, Yiguo, Li, Dan, Li, Rong
• Format: Article
• Language: English
• Subjects: A549 Cells; Adenocarcinoma - drug therapy; Adenocarcinoma - metabolism; Adenocarcinoma - pathology; Adenocarcinoma of Lung - drug therapy; Adenocarcinoma of Lung - metabolism; Adenocarcinoma of Lung - pathology; Cell migration; Cell Movement - drug effects; Cell Proliferation - drug effects; daphnetin; Humans; lung adenocarcinoma; Lung Neoplasms - drug therapy; Lung Neoplasms - metabolism; Lung Neoplasms - pathology; MAP Kinase Signaling System - drug effects; MAPK; Neoplasm Invasiveness; NF-kappa B - metabolism; Research Paper; Signal Transduction - drug effects; STAT3; STAT3 Transcription Factor - metabolism; Umbelliferones - pharmacology
• ISSN: 1933-6918; 1933-6926; 1933-6926
• DOI: 10.1080/19336918.2024.2418049

Daphnetin, a coumarin derivative isolated from Daphne odorifera, has anti-tumor effects. The MAPK, STAT3, and NF-κB signaling pathways are closely related to the pathogenesis of lung cancer. To investigate the effect of daphnetin on anti-lung adenocarcinoma A549 cells and its mechanism. The anti-tumor effects of daphnetin on the proliferation, clone formation, migration, and invasion of A549 lung adenocarcinoma cells were investigated. The results showed that daphnetin inhibited the proliferation, colony formation, migration, and invasion of A549 cells through the MAPK/STAT3/NF-KB pathway, and mainly inhibited the clonal formation and migration of A549 cells through the JNK pathway. These results provide a new research direction and theoretical basis for the use of daphnetin in the inhibition of lung adenocarcinoma.