Sparstolonin B inhibits pancreatic adenocarcinoma through the NF-xB signaling pathway

Pancreatic adenocarcinoma is a highly lethal malignant gastrointestinal tumor. Sparstolonin B is an isocoumarin whose anticancer activity has recently received increasing attention. This study aimed to investigate Sparstolonin B's potential antitumor effect on pancreatic adenocarcinoma. The effect of Sparstolonin B on pancreatic cancer target genes and molecular mechanism was predicted via network pharmacology; Sparstolonin B significantly decreased Panc-1 and SW1990 cell viability and effectively suppressed the proliferation, migration, and invasion of pancreatic cancer cells as shown by CCK-8, colony formation, and Transwell assays. Flow cytometry showed that it induced cell cycle arrest and apoptosis. Sparstolonin B also upregulated Bax levels but decreased those of MMP2 and Bcl-2, downregulated IxB alpha expression, and upregulated p65 and IxB alpha phosphorylation; however, it had no effect on total NF-xB p65 levels. The NF-xB pathway inhibitor QNZ reversed these effects. The treatment group (26 mu mol/L) had reduced graft volume and weight and fewer Ki-67-positive cells than the control group. Therefore, Sparstolonin B can inhibit the growth and induce the apoptosis of pancreatic cancer cells via the NFxB signaling pathway and may be a potential novel drug for pancreatic cancer treatment.

Automated summary

This study found that Sparstolonin B inhibits the growth and induces apoptosis of pancreatic cancer cells through the NFxB signaling pathway, making it a potential novel drug for pancreatic cancer treatment.