Sinomenine promotes ferroptosis in lung cancer cells by driving P53 gene

Abstract

Research reports have found that sinomenine has a potentially inhibitory effect on lung cancer. At the same time, sinomenine and P53 gene show a close relationship with ferroptosis. In order to further discover the mechanism of action, this research intends to evaluate whether sinomenine can drive P53 gene through DKN2A to promote the growth of iron in lung cancer. Lung cancer cells were transfected with DKN2A overexpression plasmid followed by analysis of cell proliferation, expression of DKN2A and P53. Protein expression and cell viability were observed after P53 was inhibited by the chemical inhibitor PFT-α. To further verify histological expression, epithelial injury and apoptosis expression were detected by hematoxylin and eosin stain (H&E) and immunofluorescence. Sinomenine affects activities of lung cancer cells. After sinomenine treatment, cell shape became round, with increased cell shrinkage and death. Overexpression of DKN2A inhibited sinomenine-induced ferroptosis. P53 negatively modulated DKN2A. STAT3 was upregulated with induction of ferroptosis during lung injury. In conclusion, Sinomenine promotes ferroptosis of lung cancer cells by regulating DKN2A and P53, thereby affecting the proliferation of lung cancer cell proliferation.