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Micro RNA ‐212 inhibits proliferation of gastric cancer by directly repressing retinoblastoma binding protein 2
Author(s) -
Jiping Zeng,
Ming Fang,
Lixiang Wang,
Xiuming Liang,
Yuqun Shen,
Han Yu,
Zhifang Liu,
Yundong Sun,
Shili Liu,
Chunyan Chen,
Jihui Jia
Publication year - 2013
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.24613
Subject(s) - retinoblastoma , gene knockdown , microrna , cancer , carcinogenesis , cell growth , biology , retinoblastoma protein , chemistry , cancer research , cell cycle , microbiology and biotechnology , cell culture , gene , biochemistry , genetics
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 P21 CIP1 and P27 kip1 , 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.