ArticleRedox biology2022
N-glycosylation stabilizes MerTK and promotes hepatocellular carcinoma tumor growth.
Article in Redox biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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The trial behind it
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Who cites it
38 citing papers in PubMed, 44 citations in OpenAlex.
- Structural organization of TAM receptor ectodomains.The Biochemical journal · 2026Article
- METTL7A Downregulation Drives SLC1A5-Mediated Glutamine Competition to Promote Tumor Proliferation and Suppress CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- SRD5A3-mediated aberrant N-glycosylation of SCARA5 promotes ferroptosis in lung adenocarcinoma.Oncogene · 2026Article
- N-Glycosylation of AXL Receptor Tyrosine Kinase Regulates Its Stability, Phosphorylation, and Oncogenic Function.Molecular & cellular proteomics : MCP · 2026Article
- MerTK inhibition by UNC569 triggers DNA damage and JNK/p38 MAPK cascade-driven apoptosis in pancreatic cancer.Acta biochimica et biophysica Sinica · 2026Article
- Glycolysis enzymes and cellular lactylation in tumour.Clinical and translational medicine · 2026Review
- Post-Translational Modifications of Histones and Non-Histones in Liver Disease and Traditional Chinese Medicine Treatment: A Narrative Review.Pharmacogenomics and personalized medicine · 2026Review
- Unveiling the hidden regulators: how post-translational modifications influence the progression and treatment of hepatocellular carcinoma.Frontiers in oncology · 2026Review
- MERTK inhibition improves therapeutic efficacy of immune checkpoint inhibitors in hepatocellular carcinoma.Oncoimmunology · 2025Article
- ACE-mediated Glycosylation Stabilizes PSAP To Promote GPR37-dependent Macrophage-Nucleus Pulposus Cells Crosstalk and TGFβ Signaling in Alleviating Intervertebral Disc Degeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Post-translational modifications in hepatocellular carcinoma: mechanisms and therapeutic potential.Medical oncology (Northwood, London, England) · 2025Review
- Molecular network of metabolic reprogramming and precision diagnosis and treatment of hepatocellular carcinoma.Biomarker research · 2025Review
- Glycoproteomics of Gastrointestinal Cancers and Its Use in Clinical Diagnostics.Journal of proteome research · 2025Review
- N-glycosylated LTβR increases the Th17/Treg cell ratio in liver cancer by blocking RORC ubiquitination and FOXP3 transcription.Cell death & disease · 2025Article
- Proteolysis of TAM receptors in autoimmune diseases and cancer: what does it say to us?Cell death & disease · 2025Review
- Lactate and lactylation in cancer.Signal transduction and targeted therapy · 2025Review
- Research Progress of Liver Cancer Recurrence Based on Energy Metabolism of Liver Cancer Stem Cells.Journal of hepatocellular carcinoma · 2025Review
- A multi-cohort validated OXPHOS signature predicts survival and immune profiles in grade II/III glioma patients.Frontiers in immunology · 2025Article
- Post-translational modifications in hepatocellular carcinoma: unlocking new frontiers in immunotherapy.Frontiers in immunology · 2025Review
- NSUN2-mediated mTheranostics · 2025Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite the evidences of elevated expression of Mer tyrosine kinase (MerTK) in multiple human cancers, mechanisms underlying the oncogenic roles of MerTK in hepatocellular carcinoma (HCC) remains undefined. We explored the functional effects of MerTK and N-Glycosylated MerTK on HCC cell survival and tumor growth. Here, we show that MerTK ablation increases reactive oxygen species (ROS) production and promotes the switching from glycolytic metabolism to oxidative phosphorylation in HCC cells, thus suppressing HCC cell proliferation and tumor growth. MerTK is N-glycosylated in HCC cells at asparagine 294 and 454 that stabilizes MerTK to promote oncogenic transformation. Moreover, we observed that nuclear located non-glycosylated MerTK is indispensable for survival of HCC cells under stress. Pathologically, tissue microarray (TMA) data indicate that MerTK is a pivotal prognostic factor for HCC. Our data strongly support the roles of MerTK N-glycosylation in HCC tumorigenesis and suggesting N-glycosylation inhibition as a potential HCC therapeutic strategy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.