Downregulation of miR‐199a/b‐5p is associated with GCNT2 induction upon epithelial–mesenchymal transition in colon cancer. Issue 13 (10th June 2017)

• Record Type: Journal Article
• Authors: Chao, Chia‐Chun; Wu, Po‐Han; Huang, Hsiang‐Chi; Chung, Hsiao‐Yu; Chou, Yu‐Chi; Cai, Bi‐He; Kannagi, Reiji
• Is Part Of: FEBS letters. Volume 591:Issue 13(2017)
• Page Start: 1902
• Page End: 1917
• Publication Date: 2017-06-10
• Subjects: cancer -- EMT -- GCNT2 -- I antigen glycan -- microRNA -- miR‐199; Biochemistry -- Periodicals; Biophysics -- Periodicals; Molecular biology -- Periodicals; Biochimie -- Périodiques; Biochemistry; Biophysics; Molecular biology; Periodicals; 572.05
• DOI: 10.1002/1873-3468.12685
• Languages: English
• ISSNs: 0014-5793

Abstract

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. Abstract :