Related Experiment Video
Updated: Apr 13, 2026
04:53
An In Vitro Approach to Photodynamic Therapy
Published on: August 17, 2018
8.9K
Physalin F Inhibits Cell Viability and Induces Apoptosis in Non-small Cell Lung Cancer Cells.
Jhy-Ming Li1, Kao-Tai Yang2, Chean-Ping Wu3
1Department of Animal Science, National Chiayi University, Chiayi City, Taiwan, R.O.C. jml@mail.ncyu.edu.tw.
Anticancer Research
|June 27, 2025
Summary
Physalin F, a natural compound, effectively inhibits non-small cell lung cancer (NSCLC) cell growth by inducing apoptosis and cell cycle arrest through the AKT and MAPK pathways.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Non-small cell lung cancer (NSCLC) has high mortality rates, with many patients diagnosed at advanced stages.
- Current treatments for NSCLC are limited, necessitating the development of novel therapeutic agents.
- Physalin F, a compound from *Physalis angulata* L., shows potential but its mechanisms in NSCLC are unclear.
Purpose of the Study:
- To investigate the molecular mechanisms of physalin F in NSCLC cells.
- To evaluate the therapeutic potential of physalin F against NSCLC *in vitro*.
Main Methods:
- NSCLC cell lines with wild-type or mutant EGFR were treated with physalin F.
- Cell viability was measured using CCK-8 assay.
- Apoptosis and cell-cycle progression were analyzed by flow cytometry and western blotting.
Main Results:
- Physalin F significantly reduced NSCLC cell viability and induced apoptosis via intrinsic and extrinsic pathways.
- Physalin F caused a G2/M-phase cell cycle arrest.
- Down-regulation of AKT and MAPK signaling pathways was observed; enforced AKT expression rescued physalin F's effects.
Conclusions:
- Physalin F suppresses NSCLC cell growth by inhibiting PI3K/AKT and RAS/MAPK signaling.
- Physalin F demonstrates potential as a therapeutic agent for NSCLC with both wild-type and mutant EGFR.
