| Literature DB >> 29366808 |
Rui-Lian Xu1, Wan He1, Jun Tang1, Wei Guo2, Peng Zhuang3, Chang-Qing Wang4, Wei-Ming Fu5, Jin-Fang Zhang6.
Abstract
As a primate-specific microRNA, miR-637 has been discovered for nearly 10 years. Our previous study demonstrated that miR-637 acted as a suppressor in hepatocellular carcinoma. However, its biomedical significance in pancreatic cancer remains obscure. In the present study, miR-637 was found to be significantly downregulated in pancreatic ductal adenocarcinoma (PDAC) cell lines and most of the PDAC specimens. Furthermore, the enforced overexpression of miR-637 dramatically inhibited cell proliferation and induced apoptosis of PDAC cells. Akt1, as a serine/threonine-protein kinase, has been identified as an oncogene in multiple cancers including pancreatic cancer. Our data confirmed that Akt1 was a novel target for miR-637, and its knockdown also induced cell growth inhibition and apoptosis in PDAC cells. In conclusion, our data indicated that miR-637 acted as a tumor-suppressor in PDAC, and the suppressive effect was mediated, at least partially, by suppressing Akt1 expression.Entities:
Keywords: Akt1; Apoptosis; Pancreatic ductal adenocarcinoma; Tumor-suppressor; miR-637
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Year: 2018 PMID: 29366808 DOI: 10.1016/j.yexcr.2018.01.026
Source DB: PubMed Journal: Exp Cell Res ISSN: 0014-4827 Impact factor: 3.905