TY - JOUR T1 - Silencing Delta-like 1 Expression Induces Migratory Features in Pancreatic Cancer Cells Through Stimulation of Src and p38 Signalling Pathway JF - Anticancer Research JO - Anticancer Res SP - 1335 LP - 1344 DO - 10.21873/anticanres.14075 VL - 40 IS - 3 AU - JUNGWHOI LEE AU - JUNGSUL LEE AU - DA HYE KIM AU - JAE HOON KIM Y1 - 2020/03/01 UR - http://ar.iiarjournals.org/content/40/3/1335.abstract N2 - Background/Aim: The prognosis of pancreatic cancer has not improved due to its migratory feature and refractory potential to chemo-resistance with absence of effective diagnosis. Despite continuous efforts, its underlying mechanisms of malignant nature remain ambiguous. The objective of this study was to investigate delta-like 1 (DLL1) as a tumor suppressor in the metastasic ability of human pancreatic cancer cells. Materials and Methods: Cellular expression of DLL1 was demonstrated using the GEO public database and western blot analysis. The biological function of DLL1 was validated by biological behavior analysis. Prognosis to DLL1 expression was demonstrated using analysis of the GEO public database. Results: Analysis using the GEO database and western blotting showed higher DLL1 mRNA and protein expression levels in pancreatic cancer compared to those in normal pancreas. DLL1 was uniquely expressed in seven human pancreatic cancer cell lines compared to human pancreatic duct epithelial H6c7 cells. Ablation of DLL1 expression stimulated migration and invasion by activating Src and p38 phosphorylation, but not viability and chemo-resistance of human pancreatic cancer cells. In addition, expression of DLL1 was correlated with migratory features of pancreatic cancer in vivo. Moreover, high DLL1 expression was associated with a favorable prognosis in pancreatic cancer patients. Conclusion: DLL1 is a potent suppressor of pancreatic cancer metastasis. Understanding correlation between expression and function of DLL1 might contribute to our knowledge of the complicated mechanism of pancreatic cancer metastasis. ER -