miR-148a与DNMT1之间的相互作用可能被用于胰腺癌治疗。
The Interplay Between miR-148a and DNMT1 Might be Exploited for Pancreatic Cancer Therapy.
作者信息
Zhan Qian, Fang Yuan, Deng Xiaxing, Chen Hao, Jin Jianbin, Lu Xiongxiong, Peng Chenghong, Li Hongwei, Shen Baiyong
机构信息
Department of General Surgery, Rui Jin Hospital, School of Medicine, Research Institute of Pancreatic Diseases, Shanghai Jiao Tong University , Shanghai , China.
出版信息
Cancer Invest. 2015;33(7):267-75. doi: 10.3109/07357907.2015.1025794. Epub 2015 May 7.
We discovered the expression level of miR-148a significantly decreased in pancreatic cancer tissues whereas that of DNMT1 increased. In ASPC-1 cancer cells, the overexpression of miR-148a led to a decreased level of DNMT1 and reduced the proliferation and metastasis of ASPC-1 cells. Moreover, the increased expression of miR-148a arrested the UTR methylation of p27, giving rise to an increased level of p27. Interestingly, it was shown that the DNMT1 inhibition enhanced the expression of miR-148a. In vivo studies demonstrated that the tumorigenesis of ASPC-1 was significantly arrested by either the overexpression of miR-148a or the inhibition of DNMT1.
我们发现，胰腺癌组织中miR-148a的表达水平显著降低，而DNMT1的表达水平升高。在ASPC-1癌细胞中，miR-148a的过表达导致DNMT1水平降低，并减少了ASPC-1细胞的增殖和转移。此外，miR-148a表达的增加阻止了p27的UTR甲基化，导致p27水平升高。有趣的是，研究表明DNMT1抑制增强了miR-148a的表达。体内研究表明，miR-148a的过表达或DNMT1的抑制均能显著抑制ASPC-1的肿瘤发生。
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