Ma Jia, Cao Tong, Cui Yue, Zhang Fan, Shi Ying, Xia Jun, Wang Z Peter
Department of Biochemistry and Molecular Biology, School of Laboratory Medicine, Bengbu Medical College, Anhui 233030, China.
Department of Clinical Laboratorial Examination, the First Affiliated Hospital of Bengbu Medical College, Bengbu, Anhui 233004, China.
Mol Ther Nucleic Acids. 2019 Mar 1;14:583-592. doi: 10.1016/j.omtn.2019.01.009. Epub 2019 Jan 29.
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.
新出现的证据表明，miR-223在胰腺癌（PC）进展中起关键作用；然而，其潜在机制尚未完全阐明。在本研究中，我们探讨了miR-223介导的PC肿瘤进展的分子基础。我们采用了包括MTT、FACS、转染、RT-PCR、蛋白质印迹法、Transwell和动物研究等多种方法来确定miR-223在PC细胞中的生理作用。我们发现姐妹染色单体黏连蛋白PDS5同源物B（PDS5B）是PC中miR-223的直接靶点。此外，PDS5B在PC细胞中具有肿瘤抑制功能。一致地，PDS5B的异位过表达逆转了miR-223介导的PC细胞肿瘤进展。这些结果表明，miR-223/PDS5B轴调节PC细胞的增殖和侵袭。我们的研究结果表明，miR-223的下调可能是PC的一种新的治疗方法。
