PUBLICATION

Effusanin B Inhibits Lung Cancer by Prompting Apoptosis and Inhibiting Angiogenesis

Authors
Hou, J., Li, Y., Xing, H., Cao, R., Jin, X., Xu, J., Guo, Y.
ID
ZDB-PUB-231210-3
Date
2023
Source
Molecules   28(23): (Journal)
Registered Authors
Keywords
FAK, STAT3, angiogenesis, anti-tumor, diterpenoid, effusanin B, zebrafish
MeSH Terms
  • Lung Neoplasms*/metabolism
  • Reactive Oxygen Species/metabolism
  • Cell Proliferation
  • Humans
  • Zebrafish/metabolism
  • STAT3 Transcription Factor/metabolism
  • Cell Line, Tumor
  • Apoptosis
  • Signal Transduction
  • Animals
  • Carcinoma, Non-Small-Cell Lung*/drug therapy
  • Carcinoma, Non-Small-Cell Lung*/pathology
  • Angiogenesis
PubMed
38067413 Full text @ Molecules
Abstract
Cancer is one of the deadliest human diseases, causing high rates of illness and death. Lung cancer has the highest mortality rate among all malignancies worldwide. Effusanin B, a diterpenoid derived from Isodon serra, showed therapeutic potential in treating non-small-cell lung cancer (NSCLC). Further research on the mechanism indicated that effusanin B inhibited the proliferation and migration of A549 cells both in vivo and in vitro. The in vitro activity assay demonstrated that effusanin B exhibited significant anticancer activity. Effusanin B induced apoptosis, promoted cell cycle arrest, increased the production of reactive oxygen species (ROS), and altered the mitochondrial membrane potential (MMP). Based on mechanistic studies, effusanin B was found to inhibit the proliferation and migration of A549 cells by affecting the signal transducer and activator of transcription 3 (STAT3) and focal adhesion kinase (FAK) pathways. Moreover, effusanin B inhibited tumor growth and spread in a zebrafish xenograft model and demonstrated anti-angiogenic effects in a transgenic zebrafish model.
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Human Disease / Model
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Mapping