Morusin Suppresses Pancreatic Cancer Cell Proliferation and Migration by Targeting SLC6A12 to Inhibit NF-κB and β-catenin Signaling Pathways.

introductionPancreatic cancer is characterized by a poor prognosis and low survival rate, underscoring the urgent need for the development and optimization of novel therapeutic interventions. Morusin has been reported to have anticancer activity in a variety of cancers. Therefore, the present study aimed to elucidate the anticancer effects and potential mechanisms of Morusin in pancreatic cancer.

methodsWe evaluated the anticancer effect of Morusin in pancreatic cancer cells, including its impact on pancreatic cancer cell proliferation, colony formation potential, migration, invasion, cell cycle and apoptosis. RNA sequencing (RNA-seq) analysis was employed to identify potential genes involved in the anticancer activity of Morusin. Furthermore, RT-qPCR and Western blot analysis were utilized to verify the findings.

resultsOur results demonstrated that Morusin administration significantly impaired cell proliferation, migration and invasive activity of pancreatic cancer cells. Additionally, Morusin induced apoptosis and disrupted cell cycle progression. Importantly, Morusin was found to co-regulate SLC6A12, HSPA2, P2RY6 and JPH2 in both cell lines by RNA-seq analysis, with the most significant decrease in mRNA levels of SLC6A12 following administration. Mechanistically, Morusin was found to regulate the expression of SLC6A12 and inhibit NF-κB and β-catenin signaling pathways, which may represent the underlying mechanisms of its antitumor activity.

conclusionOur findings suggest that Morusin holds potential as an anti-pancreatic cancer agent by targeting SLC6A12 and modulating its associated signaling pathways.