Why the study?
With EGFR-TKI resistance increasing, the role of ANGPTL4 in regulating gefitinib resistance in PC9/GR non-small-cell lung cancer needed investigation.
Does ANGPTL4 inhibition reduce gefitinib resistance in lung adenocarcinoma cells?
Population
A549, PC9, H1975, BEAS-2B, and PC9/GR cells and mouse transplantation tumors
Comparison
ANGPTL4 knockdown or overexpression vs controls
Design
In vitro and in vivo preclinical laboratory study
Key result
Interfering with ANGPTL4 expression in PC9/GR cells promoted sensitivity to gefitinib and mediated the NLRP3/ASC/Caspase 8 pathway to induce cell scorching and apoptosis.
Authors
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ANGPTL4 inhibition may overcome gefitinib resistance in preclinical lung adenocarcinoma models; leaves open clinical applicability.
Does ANGPTL4 inhibition reduce gefitinib resistance in lung adenocarcinoma cells?
ANGPTL4 promotes gefitinib resistance in lung adenocarcinoma cells by inhibiting pyroptosis via the NLRP3/ASC/Caspase 8 pathway, suggesting it as a potential therapeutic target.
Fang et al. (2022) studied Gefitinib resistance in non-small-cell lung cancer (NSCLC). ANGPTL4 interference/knockdown vs. Control was evaluated on Gefitinib sensitivity, cell proliferation, migration, scorching, and apoptosis. Interfering with ANGPTL4 expression in PC9/GR cells promoted sensitivity to gefitinib and mediated the NLRP3/ASC/Caspase 8 pathway to induce cell scorching and apoptosis.