DEPDC1B promotes migration and invasion in pancreatic ductal adenocarcinoma by activating the Akt/GSK3β/Snail pathway.

Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal disease, which frequently presents with distant metastasis. Further understanding of the molecular mechanism of PDAC is helpful to uncover novel and effective therapeutic strategies. DEP domain containing 1B (DEPDC1B) is known to play a role in the carcinogenesis and metastasis of several common types of cancer; however, its biological function and molecular mechanism in PDAC progression remain unclear. In the present study, the expression levels of DEPDC1B were detected in 79 pairs of PDAC and adjacent non‑cancerous tissues. Patients with PDAC that exhibited higher DEPDC1B expression levels, were shown to have a poorer prognosis. Functional studies showed that knocking down DEPDC1B inhibited PDAC cell migration and invasion, while overexpressing DEPDC1B promoted these processes. Western blotting analysis and immunofluorescence demonstrated that DEPDC1B overexpression induced the epithelial‑to‑mesenchymal transition (EMT). Further mechanistic studies revealed that DEPDC1B was able to activate the Akt/glycogen synthase kinase‑3β (GSK3β)/Snail signaling pathway. In conclusion, the results of the present study showed that DEPDC1B may serve as an oncogene that contributes to PDAC cell migration and invasion by inducing EMT via Akt/GSK3β/Snail pathway activation. [ABSTRACT FROM AUTHOR]