Department of Oncology, Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, Shenzhen 518020, PR China.
Shenzhen Ritzcon Biological Technology Co., LTD., Shenzhen, Guangdong, PR China.
Exp Cell Res. 2018 Feb 15;363(2):310-314. doi: 10.1016/j.yexcr.2018.01.026.
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.
作为一种灵长类动物特异性 microRNA，miR-637 的发现已经近 10 年了。我们之前的研究表明，miR-637 在肝细胞癌中作为一种抑制物发挥作用。然而，其在胰腺癌中的生物医学意义尚不清楚。在本研究中，我们发现 miR-637 在胰腺导管腺癌（PDAC）细胞系和大多数 PDAC 标本中显著下调。此外，miR-637 的强制过表达可显著抑制 PDAC 细胞的增殖并诱导其凋亡。Akt1 作为一种丝氨酸/苏氨酸蛋白激酶，已被确定为多种癌症（包括胰腺癌）中的致癌基因。我们的数据证实 Akt1 是 miR-637 的一个新靶标，其敲低也可诱导 PDAC 细胞的生长抑制和凋亡。总之，我们的数据表明 miR-637 在 PDAC 中发挥肿瘤抑制作用，其抑制作用至少部分是通过抑制 Akt1 表达介导的。
