Abstract
UDP-GlcNAc is a sugar substrate necessary for the O-GlcNAcylation of proteins. SLC35B4 is one of the nucleotide sugar transporters that transport UDP-GlcNAc and UDP-xylose into the endoplasmic reticulum and Golgi apparatus for glycosylation. The roles of SLC35B4 in hepatocellular carcinoma (HCC) tumorigenesis remain unknown. We find that the expression levels of SLC35B4 are higher in HCC tissues than adjacent non-tumor tissues. SLC35B4 is important for the proliferation and tumorigenesis of HCC cells. Mechanistically, SLC35B4 is important for the O-GlcNAc modification of c-Myc and thus the stabilization of c-Myc, which is required for HCC tumorigenesis. Therefore, SLC35B4 is a promising therapeutic target for treating HCC.
Highlights
IntroductionLiver cancer is one of the most common human cancers and the third leading cause of cancer death in 2020 (Sung et al, 2021)
SLC35B4 was widely expressed in hepatocellular carcinoma (HCC) cell lines, including HepG2, PLC, and 7703 cells (Figure 1E)
These findings suggest that SLC35B4 plays important roles in driving HCC development
Summary
Liver cancer is one of the most common human cancers and the third leading cause of cancer death in 2020 (Sung et al, 2021). Hepatocellular carcinoma (HCC) is the major type of primary liver cancer (Sung et al, 2021). The main risk factors causing HCC include chronic infection with hepatitis B virus or hepatitis C virus, heavy alcohol use, and non-alcoholic fatty liver disease usually associated with obesity and type 2 diabetes (Rawla et al, 2018). Available therapeutic options for HCC include tumor resection, liver transplantation, percutaneous ethanol injection, and radiofrequency ablation (Karaman et al, 2014; Llovet et al, 2021). The effective therapies for advanced HCC are limited due to the lack of understanding of the pathways driving HCC (Jeng et al, 2015). To develop more effective HCC therapy, it is important to identify new therapeutic targets that drive HCC tumorigenesis
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