Inhibition of JNK/STAT3/NF-KB pathway-mediated migration and clonal formation of lung adenocarcinoma A549 cells by daphnetin.
Humans
Cell Movement
/ drug effects
STAT3 Transcription Factor
/ metabolism
Umbelliferones
/ pharmacology
A549 Cells
Lung Neoplasms
/ metabolism
NF-kappa B
/ metabolism
Cell Proliferation
/ drug effects
Adenocarcinoma of Lung
/ metabolism
Adenocarcinoma
/ metabolism
Signal Transduction
/ drug effects
MAP Kinase Signaling System
/ drug effects
Neoplasm Invasiveness
Cell migration
MAPK
STAT3
daphnetin
lung adenocarcinoma
Journal
Cell adhesion & migration
ISSN: 1933-6926
Titre abrégé: Cell Adh Migr
Pays: United States
ID NLM: 101469464
Informations de publication
Date de publication:
Dec 2024
Dec 2024
Historique:
medline:
29
10
2024
pubmed:
29
10
2024
entrez:
29
10
2024
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 39469948
doi: 10.1080/19336918.2024.2418049
doi:
Substances chimiques
daphnetin
XC84571RD2
STAT3 Transcription Factor
0
Umbelliferones
0
NF-kappa B
0
STAT3 protein, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM