The long intergenic non-coding RNA, regulator of reprogramming (linc-ROR) is an oncogene and plays a key role in the embryonic stem cell maintenance and is involved in cancer progression. The objective of this study was to analyze linc-ROR expression in pancreatic ductal adenocarcinoma (PDAC) and determine the regulation effects of linc-ROR on proliferation and invasion of cancer cells, as well as properties of cancer stem-like cells (CSLCs). In this study, we found that linc-ROR was up-regulated in PDAC tissues and related to poor prognosis. Linc-ROR knockdown in pancreatic cancer cells inhibited cell growth and arrested in G1 phrase. Suppressed linc-ROR expression also attenuated cancer cell migration, invasion, and epithelial-mesenchymal transition. We observed that linc-ROR expression was increased in CSLCs. Importantly, linc-ROR knockdown impaired the properties and tumorigenesis of pancreatic CSLCs in vivo. Mechanistically, we found that linc-ROR functioned as a competing endogenous RNA (ceRNA) to several tumor suppressor microRNAs, particularly some members of let-7 family. We conclude that, as a crucial oncogene, linc-ROR promotes cell proliferation, invasiveness and contributes to stem cell properties of CSLCs in PDAC via acting as a ceRNA to regulate function of microRNAs. The linc-ROR is a potential therapeutic target for PDAC.