Large intergenic noncoding RNA regulator of reprogramming (Linc‐RoR) was first identified as a regulator to increase the emergence of induced pluripotent stem cells through reprogramming differentiated cells and is abnormal expression in a variety of malignant tumors. However, the function of Linc‐RoR in pancreatic cancer progression needs further clarification. The data from this study demonstrated that Linc‐RoR knockdown suppressed cell proliferative capacity and colony formation, while Linc‐RoR overexpression promoted these behaviors. In particular, Linc‐RoR overexpression promoted the level of mesenchymal markers, inhibited the expression of epithelial markers, as well as enhanced pancreatic cancer cells migration and invasion, whereas Linc‐RoR knockdown inhibited the expression of mesenchymal markers, promoted the expression of epithelial markers, as well as weakened pancreatic cancer cells migration and invasion. Further study revealed that Linc‐RoR knockdown brought about a significant fall in YAP phosphorylation and a rise in total YAP, while Linc‐RoR overexpression produced the opposite results. Specifically, Linc‐RoR promoted YAP in the cytoplasm into the nucleus. Taken together, we conjectured that Linc‐RoR promoted proliferation, migration, and invasion of pancreatic cancer cells by activating the Hippo/YAP pathway. YAP might be an underlying target of Linc‐RoR and mediate epithelial‐mesenchymal transition (EMT) in pancreatic cancer (PC); thus, Linc‐RoR might be a very meaningful biomarker for PC. Large intergenic noncoding RNA regulator of reprogramming (Linc‐RoR) promoted proliferation, migration, and invasion of pancreatic cancer cells by activating the Hippo/YAP pathway. YAP might be an underlying target of Linc‐RoR and mediate EMT in pancreatic cancer (PC); thus, Linc‐RoR might be a very meaningful biomarker for PC