DUSP28 is a novel biomarker responsible for aggravating malignancy via the autocrine signaling pathways in metastatic pancreatic cancer

Abstract

AbstractPancreatic cancer remains one of the most dangerous cancers with a grave prognosis. We previously reported that pancreatic cancer cells can secrete dual specificity phosphatise 28 (DUSP28) to the cultured medium. However, its biological function is poorly understood. Here, we have identified the function of DUSP28 in human metastatic pancreatic cancer. Treatment with recombinant DUSP28 (rDUSP28) significantly increased the migration, invasion, and viability of metastatic pancreatic cancer cells through the activation of CREB, AKT, and ERK1/2 signaling pathways. Furthermore, rDUSP28 acted as an oncogenic reagent through the interaction with integrin α1 in metastatic pancreatic cancer cells. In addition, rDUSP28 induced pro-angiogenic effects in human umbilical vein endothelial cells (HUVECs). Administration of rDUSP28 also produced tumor growth in vivo. Notably, sDUSP28 can easily be detected by immunoassay. The results establish the rationale for sDUSP28 as a promising therapeutic target and biomarker for metastatic pancreatic cancer patients.