Premium
Downregulation of miR‐199a/b‐5p is associated with GCNT 2 induction upon epithelial–mesenchymal transition in colon cancer
Author(s) -
Chao ChiaChun,
Wu PoHan,
Huang HsiangChi,
Chung HsiaoYu,
Chou YuChi,
Cai BiHe,
Kannagi Reiji
Publication year - 2017
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1002/1873-3468.12685
Subject(s) - downregulation and upregulation , epithelial–mesenchymal transition , gene silencing , colorectal cancer , gene knockdown , cancer research , antigen , chemistry , microbiology and biotechnology , cancer , cancer cell , transition (genetics) , biology , immunology , gene , biochemistry , genetics
β‐1,6‐ N ‐acetylglucosaminyltransferase 2 ( GCNT 2), which encodes a key glycosyltransferase for blood group I antigen synthesis, is induced upon epithelial–mesenchymal transition ( EMT ). Our results indicate that GCNT 2 is upregulated upon EMT induced with epidermal growth factor and basic FGF in cultured human colon cancer cells. GCNT 2 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 GCNT 2 expression in reporter assays and that it binds directly to the GCNT 2 3′ untranslated region intracellularly in RNA‐induced silencing complex‐trap assays. Overexpression of miR‐199a/b‐5p decreases GCNT 2 expression and suppresses I antigen production. Based on these findings, we propose that miR‐199a/b‐5p regulates GCNT 2 and I antigen expression in colon cancer cells undergoing EMT .