Objective: To investigate the expression of miR-526b in pancreatic cancer and its effects.  
Methods: The expressions of miR-526b in 52 specimens of pancreatic cancer and adjacent tissue as well as in different pancreatic cancer cell lines (BxPC-3, SW1990, PANC-1 and AsPC-1) and normal pancreatic ductal epithelial cells (HPDE6-C7) were determined by qRT-PCR. In pancreatic cancer cells after transfection with miR-526b mimics, miR-526b inhibitors and negative control sequences, the proliferation, invasion and apoptosis ability were examined by CCK-8, Transwell assay and flow cytometry, respectively. The potential target gene of miR-526b was analyzed by using biosoftware and dual-luciferase reporter assay, and then was verified by Western blot and qRT-PCR as well as correlation analysis.
Results: The expression levels of miR-526b in pancreatic cancer tissue was significantly lower than that in adjacent tissue, and in each pancreatic cell line was significantly lower than that in normal pancreatic ductal epithelial cell line (all P<0.05). The proliferative ability was significantly decreased, the apoptotic rate was significantly increased and the invasion ability was significantly weakened in pancreatic cells transfected with miR-526b-mimics (all P<0.05), while the opposite changes occurred in those transfected with miR-526b inhibitors (all P<0.05). The results of analysis showed that XRCC5 was a potential target gene for miR-526b; in pancreatic cells, both mRNA and protein expressions of XRCC5 were down-regulated after transfection with miR-526b mimics, and were upregulated after transfection with miR-526b inhibitors (all P<0.05); there was a negative correlation between miR-526b XRCC5 mRNA in pancreatic cancer tissue (r=–0.456, P<0.05).
Conclusion: The expression of miR-526b is down-regulated in pancreatic cancer, and the low expression of miR-526b can promote the proliferation and invasion and inhibit the apoptosis of pancreatic cancer cells. The mechanism may be related to the up-regulation of the expression of its target gene XRCC5.