期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 23, 期 22, 页码 -出版社
MDPI
DOI: 10.3390/ijms232213774
关键词
NSCLC; apoptosis; ferroptosis; ROS; PD-L1; immunotherapy
资金
- Key Discipline Construction Project of Guangdong Medical University [4SG22004G]
In this study, fascaplysin was found to inhibit migration and reverse the epithelial-mesenchymal transition phenotype by regulating the wnt/beta-catenin signaling pathway. Further research showed that fascaplysin induced ferroptosis and apoptosis in non-small cell lung cancer cells. Additionally, fascaplysin enhanced the efficacy of anti-PD-1 immunotherapy.
Fascaplysin is a natural product isolated from sponges with a wide range of anticancer activities. However, the mechanism of fascaplysin against NSCLC has not been clearly studied. In this study, fascaplysin was found to inhibit migration by regulating the wnt/beta-catenin signaling pathway and reversing the epithelial-mesenchymal transition phenotype. Further research showed that the anti-NSCLC effect of fascaplysin was mainly through the induction of ferroptosis and apoptosis. Fascaplysin-induced ferroptosis in lung cancer cells, evidenced by increased levels of ROS and Fe2+ and downregulation of ferroptosis-associated protein and endoplasmic reticulum stress, was involved in fascaplysin-induced ferroptosis. In addition, ROS was found to mediate fascaplysin-induced apoptosis. Fascaplysin significantly upregulated the expression of PD-L1 in lung cancer cells, and enhanced anti-PD-1 antitumor efficacy in a syngeneic mouse model. Therefore, these results suggest that fascaplysin exerts anticancer effects by inducing apoptosis and ferroptosis in vitro, and improving the sensitivity of anti-PD-1 immunotherapy in vivo. Fascaplysin is a promising compound for the treatment of NSCLC.
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