Journal
FEBS LETTERS
Volume 591, Issue 13, Pages 1902-1917Publisher
WILEY
DOI: 10.1002/1873-3468.12685
Keywords
cancer; EMT; GCNT2; I antigen glycan; microRNA; miR-199
Funding
- Academia Sinica
- Ministry of Science and Technology of Taiwan [MOST 104-0210-01-09-02, MOST 105-0210-01-13-01, MOST 104-2314-B-001-001, MOST 105-2320-B-001-016]
- Grants-in-Aid for Scientific Research [15K08288] Funding Source: KAKEN
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beta-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.
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