HSUEH-FEN JUANREY-HENG HUChou, Chih-HsingChih-HsingChouCHIA-LANG HSUYA-WEN LIUJOHN HUANGJI-SHIANG HUNGI-RUE LAISUNG-LIANG YUYAO-MING WUMIN-CHUAN HUANG2021-09-152021-09-1520151949-2553https://www.scopus.com/inward/record.uri?eid=2-s2.0-84925610442&doi=10.18632%2foncotarget.3117&partnerID=40&md5=a2359110c134cb836deb09e37e5b0894https://scholars.lib.ntu.edu.tw/handle/123456789/582968O-glycosylation is a common protein modification. Aberrant O-glycosylation is associated with many cancers. GALNT1 is a GalNAc-transferase that initiates protein O-glycosylation. We found that GALNT1 is frequently up-regulated in hepatocellular carcinoma (HCC) and is associated with poor patient survival. Overexpression of GALNT1 increased and knockdown decreased HCC cell migration and invasion. Knockdown of GALNT1 inhibited EGF-induced migration and invasion. Knockdown of GALNT1 decreased EGFR activation and increased EGFR degradation, by decreasing EGFR O-glycosylation. This study demonstrates that down-regulation of GALNT1 is sufficient to suppress malignant phenotype of HCC cells by decreasing EGFR signaling. Thus, GALNT1 is a potential target in HCC.en[SDGs]SDG3early endosome antigen 1; epidermal growth factor receptor; lysosome associated membrane protein 1; messenger RNA; n acetylgalactosaminyltransferase; n acetylgalactosaminyltransferase 1; unclassified drug; EGFR protein, human; epidermal growth factor receptor; n acetylgalactosaminyltransferase; polypeptide N-acetylgalactosaminyltransferase; animal experiment; animal model; animal tissue; Article; cell invasion; cell migration; cellular distribution; controlled study; female; gene expression; human; human cell; human tissue; liver cancer cell line; liver cell carcinoma; mouse; nonhuman; overall survival; protein degradation; protein glycosylation; signal transduction; upregulation; animal; antagonists and inhibitors; cell proliferation; deficiency; down regulation; gene silencing; genetic transfection; genetics; glycosylation; Hep-G2 cell line; liver cell carcinoma; liver tumor; metabolism; nonobese diabetic mouse; pathology; phenotype; physiology; SCID mouse; tumor cell line; Animals; Carcinoma, Hepatocellular; Cell Line, Tumor; Cell Proliferation; Down-Regulation; Female; Gene Knockdown Techniques; Glycosylation; Hep G2 Cells; Humans; Liver Neoplasms; Mice; Mice, Inbred NOD; Mice, SCID; N-Acetylgalactosaminyltransferases; Phenotype; Receptor, Epidermal Growth Factor; Signal Transduction; Transfection; Up-Regulationjournal article10.18632/oncotarget.3117257309042-s2.0-84925610442