机构：[1]Department of Oncology, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, Shenzhen 518020, PR China深圳市康宁医院深圳市人民医院深圳医学信息中心[2]Shenzhen Ritzcon Biological Technology Co., LTD., Shenzhen, Guangdong, PR China[3]Department of Infectious Disease, The Eighth Affiliated Hospital, Sun Yat-sen University, Shenzhen 518033, PR China深圳市康宁医院深圳医学信息中心中国医学科学院阜外医院深圳医院[4]Department of Oncology, The People's Hospital of Baoan Shenzhen, Shenzhen 518101, PR China深圳市宝安区人民医院深圳市康宁医院深圳市人民医院深圳医学信息中心[5]Guangdong Provincial Key Laboratory of New Drug Screening, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, Guangdong, PRChina[6]School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, Guangdong, PR China[7]Key Laboratory of Orthopaedics and Traumatology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, The First Clinical Medical College,Guangzhou University of Chinese Medicine, Guangzhou, PR China
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.
基金：
National Natural Science Foundation of ChinaNational Natural Science Foundation of China [81773066, 81772404]
第一作者机构：[1]Department of Oncology, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, Shenzhen 518020, PR China
通讯作者：
通讯机构：[5]Guangdong Provincial Key Laboratory of New Drug Screening, School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, Guangdong, PRChina[6]School of Pharmaceutical Sciences, Southern Medical University, Guangzhou 510515, Guangdong, PR China[*1]School of Medicine, Southern Medical University, Guangzhou, PR China.
推荐引用方式(GB/T 7714)：
Xu Rui-lian,He Wan,Tang Jun,et al.Primate-specific miRNA-637 inhibited tumorigenesis in human pancreatic ductal adenocarcinoma cells by suppressing Akt1 expression[J].EXPERIMENTAL CELL RESEARCH.2018,363(2):310-314.doi:10.1016/j.yexcr.2018.01.026.
APA：
Xu, Rui-lian,He, Wan,Tang, Jun,Guo, Wei,Zhuang, Peng...&Zhang, Jin-fang.(2018).Primate-specific miRNA-637 inhibited tumorigenesis in human pancreatic ductal adenocarcinoma cells by suppressing Akt1 expression.EXPERIMENTAL CELL RESEARCH,363,(2)
MLA：
Xu, Rui-lian,et al."Primate-specific miRNA-637 inhibited tumorigenesis in human pancreatic ductal adenocarcinoma cells by suppressing Akt1 expression".EXPERIMENTAL CELL RESEARCH 363..2(2018):310-314
