Regulation of actin-binding protein ANLN by antitumor miR-217 inhibits cancer cell aggressiveness in pancreatic ductal adenocarcinoma

Analysis of our microRNA (miRNA) expression signature of pancreatic ductal adenocarcinoma (PDAC) revealed that ( ) was significantly reduced in cancer tissues. The aim of this study was to investigate the antitumor roles of in PDAC cells and to identify -mediated molecular pathways involved in PDAC aggressiveness. The expression levels of were significantly reduced in PDAC clinical specimens. Ectopic expression of significantly suppressed cancer cell migration and invasion. Transcription of actin-binding protein Anillin (coded by ) was detected by our and gene expression analyses. Moreover, luciferase reporter assays showed that was a direct target of in PDAC cells. Overexpression of was detected in PDAC clinical specimens by real-time PCR methods and immunohistochemistry. Interestingly, Kaplan-Meier survival curves showed that high expression of predicted shorter survival in patients with PDAC by TCGA database analysis. Silencing expression markedly inhibited cancer cell migration and invasion capabilities of PDAC cell lines. We further investigated -mediated downstream pathways in PDAC cells. "Focal adhesion" and "Regulation of actin binding protein" were identified as -modulated downstream pathways in PDAC cells. Identification of antitumor / -mediated PDAC pathways will provide new insights into the potential mechanisms underlying the aggressive course of PDAC.