Curcumin induces ferroptosis in non‐small‐cell lung cancer via activating autophagy

• DOI: 10.1111/1759-7714.13904
• Publication Date: 2021-03-03T13:45:19Z
• Authors: Xin Tang; Hui Ding; Maoli Liang; Xing Chen; Yuxia Yan; Nansheng Wan; Qianqian Chen; Jing Zhang; Jie Cao
• Keywords: Viability assay

Abstract Background Emerging studies showed curcumin can inhibit glioblastoma and breast cancer cells via regulating ferroptosis. However, the role of ferroptosis in inhibitory effect on non‐small‐cell lung (NSCLC) remains unclear. Methods Cell counting kit‐8 (CCK‐8) assay was used to measure viability A549 H1299 under different conditions. proliferation examined by Ki67 immunofluorescence. The morphological changes tumor tissues were observed optical microscope hematoxylin eosin (H&E) staining. Intracellular reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), iron contents determined corresponding kit. related protein expression levels detected western blot immunohistochemistry. Transmission electron observe ultrastructure cells. Results Curcumin inhibited growth cell proliferation, but promoted death. Characteristic group, including overload, GSH depletion lipid peroxidation. Meanwhile, level ACSL4 higher SLC7A11 GPX4 lower group than that control group. Incubation inhibitors ferrostatin‐1 (Fer‐1) or knockdown iron‐responsive element‐binding 2 (IREB2) notably weakened curcumin‐induced anti‐tumor Further investigation suggested induced mitochondrial membrane rupture cristae decrease, increased autolysosome, Beclin1 LC3, decreased P62. Curcumin‐induced autophagy subsequent both alleviated with inhibitor chloroquine (CQ) siBeclin1. Conclusion activating NSCLC, which enhanced therapeutic NSCLC.