O-GlcNAcylation promotes colorectal cancer metastasis via the miR-101-O-GlcNAc/EZH2 regulatory feedback circuit View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-01

AUTHORS

Mingzuo Jiang, Bing Xu, Xiaowei Li, Yulong Shang, Yi Chu, Weijie Wang, Di Chen, Nan Wu, Sijun Hu, Song Zhang, Mengbin Li, Kaichun Wu, Xiaoyong Yang, Jie Liang, Yongzhan Nie, Daiming Fan

ABSTRACT

Advanced colorectal cancer (CRC) is one of the deadliest cancers, and the 5-year survival rate of patients with metastasis is extremely low. The epithelial-mesenchymal transition (EMT) is considered essential for metastatic CRC, but the fundamental molecular basis underlying this effect remains unknown. Here, we identified that O-GlcNAcylation, a unique posttranslational modification (PTM) involved in cancer metabolic reprogramming, increased the metastatic capability of CRC. The levels of O-GlcNAcylation were increased in the metastatic CRC tissues and cell lines, which likely promoted the EMT by enhancing EZH2 protein stability and function. The CRC patients with higher levels of O-GlcNAcylation exhibited greater lymph node metastasis potential and lower overall survival. Bioinformatic analysis and luciferase reporter assays revealed that both O-GlcNAcylation transferase (OGT) and EZH2 are posttranscriptionally inhibited by microRNA-101. In addition, O-GlcNAcylation and H3K27me3 modification in the miR-101 promoter region further inhibited the transcription of miR-101, resulting in the upregulation of OGT and EZH2 in metastatic CRC, thus forming a vicious cycle. In this study, we demonstrated that O-GlcNAcylation, which is negatively regulated by microRNA-101, likely promotes CRC metastasis by enhancing EZH2 protein stability and function. Reducing O-GlcNAcylation may be a potential therapeutic strategy for metastatic CRC. More... »

PAGES

301-316

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41388-018-0435-5

    DOI

    http://dx.doi.org/10.1038/s41388-018-0435-5

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1106061404

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30093632


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