PT  - JOURNAL ARTICLE
AU  - LI, JHY-MING
AU  - YANG, KAO-TAI
AU  - WU, CHEAN-PING
TI  - Physalin F Inhibits Cell Viability and Induces Apoptosis in Non-small Cell Lung Cancer Cells
AID  - 10.21873/anticanres.17668
DP  - 2025 Jul 01
TA  - Anticancer Research
PG  - 3031--3044
VI  - 45
IP  - 7
4099  - http://ar.iiarjournals.org/content/45/7/3031.short
4100  - http://ar.iiarjournals.org/content/45/7/3031.full
SO  - Anticancer Res2025 Jul 01; 45
AB  - Background/Aim: Lung cancer has a high morbidity rate and remains the leading cause of mortality worldwide. Most patients with non-small cell lung cancer (NSCLC) are diagnosed at advanced stages, rendering surgical resection unfeasible and prognosis poor. Therefore, effective therapeutic agents for NSCLC are urgently needed. Physalin F, a steroid derivative isolated from Physalis angulata L., reduces cancer cell viability through unclear mechanisms. This study investigated the molecular mechanisms and therapeutic potential of physalin F in NSCLC cells in vitro.Materials and Methods: Four NSCLC cell lines, harboring either wild-type (H460 and A549) or mutant (H1650 and H1975) EGFR, were treated with various concentrations of physalin F. Cell viability was assessed using the CCK-8 reagent. Apoptosis and cell-cycle progression were analyzed via flow cytometry and western blotting.Results: Physalin F significantly inhibited cell viability and induced apoptosis through the intrinsic and extrinsic pathways in NSCLC cells. It caused G2/M-phase cell cycle arrest. Mechanistically, physalin F down-regulated AKT and MAPK signaling pathways. Conversely, enforced AKT expression reversed physalin F-induced suppression of cell viability in NSCLC cells.Conclusion: Physalin F suppresses NSCLC cell growth via PI3K/AKT and RAS/MAPK signaling pathways. These findings suggest that physalin F holds potential as an effective therapeutic agent for NSCLC harboring both wild-type and mutant EGFR.