<?xml version='1.0' encoding='UTF-8'?><xml><records><record><source-app name="HighWire" version="7.x">Drupal-HighWire</source-app><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">LI, JHY-MING</style></author><author><style face="normal" font="default" size="100%">YANG, KAO-TAI</style></author><author><style face="normal" font="default" size="100%">WU, CHEAN-PING</style></author></authors><secondary-authors></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">Physalin F Inhibits Cell Viability and Induces Apoptosis in Non-small Cell Lung Cancer Cells</style></title><secondary-title><style face="normal" font="default" size="100%">Anticancer Research</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2025</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2025-07-01 00:00:00</style></date></pub-dates></dates><pages><style  face="normal" font="default" size="100%">3031-3044</style></pages><doi><style  face="normal" font="default" size="100%">10.21873/anticanres.17668</style></doi><volume><style face="normal" font="default" size="100%">45</style></volume><issue><style face="normal" font="default" size="100%">7</style></issue><abstract><style  face="normal" font="default" size="100%">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.</style></abstract></record></records></xml>