Acylglycerol kinase contributes to cell proliferation by activating NF‑κB signaling pathway in pancreatic cancer

Pancreatic Cancer mortality remains high due to late diagnosis and therapeutic resistance. The present study investigated acylglycerol kinase (AGK), which has been implicated in other Tumors, in Pancreatic Cancer. Quantitative PCR, western blotting and immunohistochemistry analyses showed that AGK was markedly upregulated in Pancreatic Cancer tissues and cell lines and its expression associated with poor prognosis. Furthermore, functional studies using AGK knockdown and overexpression models demonstrated that AGK promoted Cancer cell proliferation by upregulating proliferation‑associated genes, such as MYC, MKI67 and CCNB1. Mechanistically, AGK activates NF‑κB signaling pathway by facilitating p65 nuclear translocation and enhancing its phosphorylation. Additionally, CCK‑8 and colony formation assays further indicated that elevated AGK levels reduced sensitivity to therapeutic drugs and irradiation in Pancreatic Cancer cells. These findings revealed the critical role of AGK in Pancreatic Cancer progression and treatment resistance, identifying it as a potential novel therapeutic target and diagnostic marker.