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A novel regulatory circuit of miR‑152 and DNMT1 in human bladder cancer.

Authors: Zhang, Haiqing  Qi, Defeng  Li, Jinhui  Peng, Tao  Yang, Linqing  Yuan, Jianhui  Zhang, Yuying  Hu, Yuan  Su, Jialin  Que, Biao  Li, Mengxi  Zhou, Guoren  Chen, Yuxin  Zhang, Wenjuan  Ji, Weidong 
Citation: Zhang H, etal., Oncol Rep. 2018 Sep;40(3):1803-1812. doi: 10.3892/or.2018.6553. Epub 2018 Jul 10.
Pubmed: (View Article at PubMed) PMID:30015946
DOI: Full-text: DOI:10.3892/or.2018.6553

Downregulation of microRNA‑152 (miR‑152) has been observed in various types of human malignancies, including Bladder cancer (BC). However, the role of miR‑152 in the development and progression of BC is still unclear. In our previous study, we identified a functional crosstalk between miR‑152 and DNA methyltransferase 1 (DNMT1) involved in Nis‑induced malignant transformation. In the present study, we found that the expression of miR‑152 was specifically downregulated in BC cells and tissues via the DNA hypermethylation of the miR‑152 promoter. The overexpression of miR‑152 in BC cells resulted in a reduction of DNMT1, whereas the inhibition of the expression of miR‑152 induced an elevated level of DNMT1. Further studies revealed that miR‑152 directly downregulated the expression of DNMT1 by targeting the 3'‑UTR of its transcript in BC cells. In addition, ectopic expression of miR‑152 in BC cells significantly inhibited cell proliferation, whereas the inhibition of miR‑152 expression led to increased cell proliferation. These findings indicated a novel regulatory circuit of miR‑152/DNMT1 in BC, and more importantly, the combination of miR‑152 and DNMT1 may function as promising therapeutic modalities and early biomarkers for BC.


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RGD Object Information
RGD ID: 19165141
Created: 2020-02-04
Species: All species
Last Modified: 2020-02-04
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.