ArticleFrontiers in pharmacology2022
SLC35B4 Stabilizes c-MYC Protein by O-GlcNAcylation in HCC.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- FOXK1: a multifaceted regulator in metabolic reprogramming and disease progression.Biology direct · 2026Review
- miRNA‑29a inhibits the proliferation of HUVECs by regulating the ITGB1/β‑catenin/c‑Myc pathway.Molecular medicine reports · 2026Article
- Article
- Polycyclic aromatic hydrocarbon derivative 3-hydroxybenz[a]anthracene promotes the progression of T47D breast cancer cells by modulating relevant protein expression.Frontiers in cell and developmental biology · 2026Article
- Current Advancements in Serum Protein Biomarkers for Hepatitis B Virus-Associated Hepatocyte Remodeling and Hepatocellular Carcinoma.Immunity, inflammation and disease · 2025Review
- Regulatory factor X-5/SCL/TAL1 interruption site axis promotes aerobic glycolysis and hepatocellular carcinoma cell stemness.The Kaohsiung journal of medical sciences · 2025Article
- Protein glycosylation alterations in hepatocellular carcinoma: function and clinical implications.Oncogene · 2023Review
- Article
- Metabolite-derived protein modifications modulating oncogenic signaling.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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