Department of Biochemistry and Molecular Biology, School of Laboratory Medicine, Bengbu Medical College, Anhui 233030, China; Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA. Electronic address: [Email]
Emerging evidence has demonstrated that miR-223 is critically involved in the progression of pancreatic cancer (PC); however, the underlying mechanisms are not fully elucidated. In the present study, we explored the molecular basis of miR-223-mediated tumor progression in PC. We performed numerous approaches including MTT, FACS, transfection, RT-PCR, western blotting, Transwell, and animal studies to determine the physiological role of miR-223 in PC cells. We found that sister chromatid cohesion protein PDS5 homolog B (PDS5B) is a direct target of miR-223 in PC. Moreover, PDS5B exhibits tumor-suppressive function in PC cells. Consistently, ectopic overexpression of PDS5B reversed miR-223-mediated tumor progression in PC cells. These results suggest that the miR-223/PDS5B axis regulates cell proliferation and invasion in PC cells. Our findings indicated that downregulation of miR-223 could be a novel therapeutic approach for PC.