DNA demethylases of the TET family function as tumor suppressors in various human cancers, but their pathogenic contributions and mechanisms of action in gastric carcinogenesis and progression remain unclear. Here, we report that TET is transcriptionally upregulated in gastric cancer, where it correlates with poor prognosis. Mechanistic investigations revealed that TET facilitated gastric carcinogenesis through a noncoding function of the 3'UTR, which interacted with miR-26. This interaction resulted in sequestration of miR-26 from its target EZH2, which released the suppression on EZH2, and thereby led to EZH2 overexpression in gastric cancer. Our findings uncover a novel noncoding function for TET family proteins in facilitating gastric carcinogenesis. Cancer Res; 77(22); 6069-82. ©2017 AACR.
TET-Mediated Sequestration of miR-26 Drives EZH2 Expression and Gastric Carcinogenesis.
M. Deng,Ruixin Zhang,Zhengxi He,Q. Qiu,Xihong Lu,Jiang Yin,Hao Liu,X. Jia,Zhiming He
Published 2017 in Cancer Research
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- Publication year
2017
- Venue
Cancer Research
- Publication date
2017-11-15
- Fields of study
Biology, Medicine
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- Source metadata
Semantic Scholar, PubMed
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