Chrysophanol inhibits the progression of gastric cancer by activating nod-like receptor protein-3

Abstract

Aim: Gastric cancer (GC) is one of the most common malignant tumors. Chrysophanol has been reported to possess antitumor effects on a variety of cancers; however, its role in GC remains unclear. This study aimed to investigate the effects of chrysophanol on the proliferation, pyroptosis, migration, and invasion of GC cells. Methods: Human GC cell lines MKN 28 and AGS cells were treated with different concentrations of chrysophanol, then cell proliferation, migration, invasion and pyroptosis were determined by CCK-8, colony-forming assay, wound healing assay, Transwell assay, and flow cytometry. Cell migration and invasion were reassessed in these transfected cells following the transfection of nod-like receptor protein-3 (NLRP3) siRNA in MKN 28 and AGS cells. To examine the downstream signaling pathway of the NLRP3 signaling pathway, NLRP3, caspase-1, gasdermin-D, interleukin (IL)-1β, and IL-18 were detected by quantitative real-time-polymerase chain reaction or western blotting. Results: Chrysophanol inhibited the proliferation of GC cells, caused pyroptosis, inhibited cell migration and invasion, and increased the expression of NLRP3 inflammasomes in GC cells. Knockdown of NLRP3 inhibited the effects of chrysophanol on proliferation, pyroptosis, migration, and invasion of GC cells. Chrysophanol plays an anticancer role by enhancing NLRP3. Conclusions: Chrysophanol exerts anti-neoplastic effects in vitro in GC cells by modulating NLRP3, thus highlighting its therapeutic potential in GC.