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Due to its aggressive nature, pancreatic ductal adenocarcinoma ( PDAC ) is one of the most lethal and hard‐to‐treat malignancies. Recently developed targeted molecular strategies have contributed to remarkable improvements in the treatment of several cancers. However, such therapies have not been applied to  PDAC . Therefore, new treatment options are needed for  PDAC  based on current genomic approaches. Expression of  micro RNA ‐375  ( miR‐375 ) was significantly reduced in mi RNA  expression signatures of several types of cancers, including  PDAC . The aim of the present study was to investigate the functional roles of  miR‐375  in  PDAC  cells and to identify  miR‐375 ‐regulated molecular networks involved in  PDAC  aggressiveness. The expression levels of  miR‐375  were markedly downregulated in  PDAC  clinical specimens and cell lines ( PANC ‐1 and  SW 1990). Ectopic expression of  miR‐375  significantly suppressed cancer cell proliferation, migration and invasion. Our  in silico  and gene expression analyses and luciferase reporter assay showed that zinc finger protein 36 ring finger protein‐like 2 (  ZFP 36L2 ) was a direct target of  miR‐375  in  PDAC  cells. Silencing   ZFP 36L2  inhibited cancer cell aggressiveness in  PDAC  cell lines, and overexpression of  ZFP 36L2 was confirmed in  PDAC  clinical specimens. Interestingly, Kaplan–Meier survival curves showed that high expression of  ZFP 36L2 predicted shorter survival in patients with  PDAC . Moreover, we investigated the downstream molecular networks of the  miR‐375/ ZFP 36L2  axis in  PDAC  cells. Elucidation of tumor‐suppressive  miR‐375 ‐mediated  PDAC  molecular networks may provide new insights into the potential mechanisms of  PDAC  pathogenesis.

ZFP 36L2 promotes cancer cell aggressiveness and is regulated by antitumor micro RNA ‐375 in pancreatic ductal adenocarcinoma