Abstract 1402: Silencing of B4GALT1 inversely regulates malignant phenotypes of hepatocellular carcinoma cells

Abstract

Abstract Identifying molecular targets for hepatocellular carcinoma (HCC) is an urgent need to overcome the treatment failure and death from cancer cell invasion and metastasis. Beta-1,4-galactosyltransferase 1 (B4GALT1) has been documented as the key enzyme in morphogenesis and cellular adhesion, for it adds galactose to N-acetylglucosamine residues of glycoprotein carbohydrate chains; whereas abnormal B4GALT1 expression is associated with tumor progress in many cancers. However, functional roles of B4GALT1 in HCC remains unclear. With clinical correlation, the immunohistochemistry confirmed that lower expression of B4GALT1 in cancer tissue is associated with higher ratio of vascular invasion and worse overall survival. Consistently, stable knockdown of B4GALT1 regarding HCC cell lines promoted cell migration, and invasion; as the overexpressed B4GALT1 inhibited cell migration and invasion of HCC cell lines. Moreover, our data suggested that down-regulated B4GALT1 modified LEL lectin, and interfered hepatocyte growth factor receptor (HGFR), Epidermal growth factor receptor (EGFR), and Axl signaling. Given that, B4GALT1 is sufficient to inversely regulate malignant behaviors of HCC cells with a significant correlation between gene expression and clinical prognosis, implying that B4GALT1 played a crucial role in cancer progress of HCC. Citation Format: Po-Da Chen, Ai-An Chang, Yao-Ming Wu, Min-Chuan Huang. Silencing of B4GALT1 inversely regulates malignant phenotypes of hepatocellular carcinoma cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1402.