RT Journal Article
SR Electronic
T1 Physalin F Inhibits Cell Viability and Induces Apoptosis in Non-small Cell Lung Cancer Cells
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 3031
OP 3044
DO 10.21873/anticanres.17668
VO 45
IS 7
A1 LI, JHY-MING
A1 YANG, KAO-TAI
A1 WU, CHEAN-PING
YR 2025
UL http://ar.iiarjournals.org/content/45/7/3031.abstract
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.