期刊
FEBS LETTERS
卷 591, 期 13, 页码 1902-1917出版社
WILEY
DOI: 10.1002/1873-3468.12685
关键词
cancer; EMT; GCNT2; I antigen glycan; microRNA; miR-199
资金
- 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
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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