TET-Mediated Sequestration of miR-26 Drives EZH2 Expression and Gastric Carcinogenesis.
basic_science · Level V
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- Record sourced from PubMed, PMID 28923852.
- Also identified by DOI 10.1158/0008-5472.CAN-16-2964.
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Abstract
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. <i>Cancer Res; 77(22); 6069-82. ©2017 AACR</i>.
Medical subject headings
- DNA-Binding Proteins
- Dioxygenases
- Enhancer of Zeste Homolog 2 Protein
- MicroRNAs
- Mixed Function Oxygenases
- Proto-Oncogene Proteins
- Stomach Neoplasms