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Long noncoding  RNA  (lnc RNA )   DLEU 2  has been shown to be dysregulated in several type of tumor. However, the potential biological roles and molecular mechanisms of   DLEU 2  in pancreatic cancer ( PC ) progression are poorly understood. In this study, we found that the   DLEU 2  level was substantially upregulated in  PC  tissues and  PC  cell lines, and significantly associated with poor clinical outcomes in  PC  patients. Overexpression of  DLEU 2 significantly induced  PC  cell proliferation and invasion, whereas knockdown of  DLEU 2 impaired cell proliferation and invasion in vitro. Furthermore, bioinformatics analysis, luciferase reporter assay, and  RNA  immunoprecipitation assay revealed that  DLEU 2 directly bond to microRNA‐455 (miR‐455) and functioned as an endogenous sponge for miR‐455, which could remarkably suppress cell growth and invasion. We also determined that  SMAD 2 was a direct target of miR‐455, and the restoration of  SMAD 2 rescued cell growth and invasion that were reduced by  DLEU 2 knockdown or miR‐455 overexpression. In addition, low miR‐455 expression and high  SMAD 2 expression was correlated with poor patient survival. These results indicate that  DLEU 2 is an important promoter of  PC  development, and targeting the  DLEU 2/miR‐455/ SMAD 2 pathway could be a promising therapeutic approach in the treatment of  PC .

Silencing of DLEU 2 suppresses pancreatic cancer cell proliferation and invasion by upregulating microRNA‐455