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FEBS Lett. 2017 Jul;591(13):1902-1917. doi: 10.1002/1873-3468.12685. Epub 2017 Jun 10.

Downregulation of miR-199a/b-5p is associated with GCNT2 induction upon epithelial-mesenchymal transition in colon cancer.

Author information

1
Graduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan.
2
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
3
Taiwan International Graduate Program in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei, Taiwan.
4
Genomics Research Center, Academia Sinica, Taipei, Taiwan.
5
National RNAi Core Facility, Academia Sinica, Taipei, Taiwan.
6
Department of Biology and Anatomy, National Defense Medical Center, Taipei, Taiwan.

Abstract

β-1,6-N-acetylglucosaminyltransferase 2 (GCNT2), which encodes a key glycosyltransferase for blood group I antigen synthesis, is induced upon epithelial-mesenchymal transition (EMT). Our results indicate that GCNT2 is upregulated upon EMT induced with epidermal growth factor and basic FGF in cultured human colon cancer cells. GCNT2 knockdown or overexpression decreases or increases, respectively, malignancy-related characteristics of colon cancer cells and I antigen levels. MiR-199a/b-5p is markedly downregulated upon EMT in colon cancer cells. Here, we find that miR-199a/b-5p consistently regulates GCNT2 expression in reporter assays and that it binds directly to the GCNT2 3' untranslated region intracellularly in RNA-induced silencing complex-trap assays. Overexpression of miR-199a/b-5p decreases GCNT2 expression and suppresses I antigen production. Based on these findings, we propose that miR-199a/b-5p regulates GCNT2 and I antigen expression in colon cancer cells undergoing EMT.

KEYWORDS:

EMT ; GCNT2; I antigen glycan; cancer; miR-199; microRNA

PMID:
28542779
DOI:
10.1002/1873-3468.12685
[Indexed for MEDLINE]
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