ZJ, FM, and JJ designed the study; ZJ, FM, WL, SY, and LX performed the study; ZJ, FM, WL, LX, YH, LZ, and SY analyzed and interpreted the data; CC and JJ supervised the study; and ZJ, FM and JJ wrote the paper.
MicroRNA-212 inhibits proliferation of gastric cancer by directly repressing retinoblastoma binding protein 2
Article first published online: 15 OCT 2013
© 2013 Wiley Periodicals, Inc.
Journal of Cellular Biochemistry
Volume 114, Issue 12, pages 2666–2672, December 2013
How to Cite
Jiping, Z., Ming, F., Lixiang, W., Xiuming, L., Yuqun, S., Han, Y., Zhifang, L., Yundong, S., Shili, L., Chunyan, C. and Jihui, J. (2013), MicroRNA-212 inhibits proliferation of gastric cancer by directly repressing retinoblastoma binding protein 2. J. Cell. Biochem., 114: 2666–2672. doi: 10.1002/jcb.24613
Conflicts of interest: No conflicts of interest were declared.
This manuscript has not been published in whole or in part nor is it being considered for publication elsewhere.
Zeng Jiping and Fang Ming contributed equally to this work.
- Issue published online: 15 OCT 2013
- Article first published online: 15 OCT 2013
- Accepted manuscript online: 21 JUN 2013 02:35PM EST
- Manuscript Accepted: 11 JUN 2013
- Manuscript Received: 8 MAR 2013
- National Basic Research Program of China. Grant Number: 973 Program 2012CB911202
- National Natural Science Foundation of China. Grant Numbers: 81001098, 81171536, 81170514, 81172354, 81272654
- Science Foundation of Shandong Province. Grant Numbers: ZR2010HZ003, ZR2010HQ020
- GASTRIC CANCER;
Retinoblastoma binding protein 2 (RBP2), a newly found histone demethylase, is overexpressed in gastric cancer. We examined the upstream regulatory mechanism of RBP2 at the microRNA (miRNA) level and the role in gastric carcinogenesis. We used bioinformatics to predict that microRNA-212 (miR-212) might be a direct upstream regulator of RBP2 and verified the regulation in gastric epithelial-derived cell lines. Overexpression of miR-212 significantly inhibited the expression levels of RBP2, whereas knockdown of miR-212 promoted RBP2 expression. Furthermore, we identified the putative miR-212 targeting sequence in the RBP2 3′ UTR by luciferase assay. MiR-212 inhibited the colony formation ability of cells by repressing RBP2 expression and increasing that of P21CIP1 and P27kip1, both critical in cell cycle arrest. In addition, the expression of RBP2 and miR-212 in tumor tissue and matched normal tissue from 18 patients further supported the results in vivo. MiR-212 directly regulates the expression of RBP2 and inhibits cell growth in gastric cancer, which may provide new clues to treatment. J. Cell. Biochem. 114: 2666–2672, 2013. © 2013 Wiley Periodicals, Inc.