Chou Chih-Hsing, Huang Miao-Juei, Chen Chi-Hau, Shyu Ming-Kwang, Huang John, Hung Ji-Shiang, Huang Chiun-Sheng, Huang Min-Chuan
Graduate Institute of Anatomy and Cell Biology, National Taiwan University College of Medicine, Taipei, Taiwan.
Department of Obstetrics and Gynecology, National Taiwan University Hospital, Taipei, Taiwan.
Oncotarget. 2015 Mar 20;6(8):6123-35. doi: 10.18632/oncotarget.3045.
Aberrant glycosylation is frequently observed in cancers. Core 1 β1,3-galactosyltransferase (C1GALT1) is an exclusive enzyme in humans that catalyzes the biosynthesis of core 1 O-glycan structure, Gal-GalNAc-O-Ser/Thr, whose expression is commonly up-regulated during tumorigenesis. Little is known about the function of C1GALT1 in breast cancer. This study aims to determine the correlation between C1GALT1 expression and breast cancer clinicopathological features and roles of C1GALT1 in breast cancer malignant phenotypes. Public databases and our data showed that C1GALT1 mRNA and C1GALT1 protein are frequently up-regulated in breast cancer; and increased C1GALT1 expression correlates with higher histological grade and advanced tumor stage. Overexpression of C1GALT1 enhanced breast cancer cell growth, migration, and invasion in vitro as well as tumor growth in vivo. Conversely, C1GALT1 knockdown suppressed these malignant phenotypes. Furthermore, C1GALT1 modulates O-glycan structures on Mucin (MUC) 1 and promotes MUC1-C/β-catenin signaling in breast cancer cells. These findings suggest that C1GALT1 enhances breast cancer malignant progression through promoting MUC1-C/β-catenin signaling pathway. Unveiling the function of C1GALT1 in breast cancer opens new insights to the roles of C1GALT1 and O-glycosylation in tumorigenesis and renders the potential of C1GALT1 as a target of novel therapeutic agent development.
异常糖基化在癌症中经常被观察到。核心1 β1,3-半乳糖基转移酶(C1GALT1)是人类中一种独特的酶,它催化核心1 O-聚糖结构Gal-GalNAc-O-Ser/Thr的生物合成,其表达在肿瘤发生过程中通常上调。关于C1GALT1在乳腺癌中的功能知之甚少。本研究旨在确定C1GALT1表达与乳腺癌临床病理特征之间的相关性以及C1GALT1在乳腺癌恶性表型中的作用。公共数据库和我们的数据显示,C1GALT1 mRNA和C1GALT1蛋白在乳腺癌中经常上调;C1GALT1表达增加与更高的组织学分级和晚期肿瘤分期相关。C1GALT1的过表达增强了乳腺癌细胞在体外的生长、迁移和侵袭以及在体内的肿瘤生长。相反,C1GALT1的敲低抑制了这些恶性表型。此外,C1GALT1调节粘蛋白(MUC)1上的O-聚糖结构,并促进乳腺癌细胞中的MUC1-C/β-连环蛋白信号传导。这些发现表明,C1GALT1通过促进MUC1-C/β-连环蛋白信号通路增强乳腺癌的恶性进展。揭示C1GALT1在乳腺癌中的功能为C1GALT1和O-糖基化在肿瘤发生中的作用提供了新的见解,并使C1GALT1作为新型治疗药物开发靶点的潜力得以显现。