ArticleCell death & disease2025
S100A2 promotes clear cell renal cell carcinoma tumor metastasis through regulating GLUT2 expression.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Metabolic reprogramming in cancer: dysregulation of glucose, lipid, and amino acid pathways and therapeutic opportunities.Molecular biomedicine · 2026Review
- Metabolic reprogramming in cancer: signaling pathways and therapeutic targets.Molecular cancer · 2026Review
- Metabolic Messengers: Extracellular Vesicles as Central Mediators of Metabolic Reprogramming in Renal Cell Cancer.Biomedicines · 2026Review
- HDAC6 orchestrates metastatic and immunosuppressive programs in small cell lung cancer through S100A2-TGF-β/SMAD and CSF1R signaling.Molecular cancer · 2026Article
- Obesity-driven metabolic reprogramming and immune dysfunction in renal cancer.Frontiers in immunology · 2026Review
- Molecular regulatory network of glycolytic reprogramming in hepatocellular carcinoma and its clinical implications.Biological procedures online · 2025Review
- Clinical Risk Stratification and Modifiable Risk Factors for Hepatitis B Virus-Related Follicular Lymphoma.ImmunoTargets and therapy · 2025Article
- Emerging roles of metabolic biomarkers in renal cell carcinoma: from molecular mechanisms to clinical implications.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
12 authors.
Funding
Abstract
Clear cell renal cell carcinoma (ccRCC) is the predominant subtype of renal cancer and is highly malignant. Despite advances in diagnostics and treatment, the prognosis for ccRCC remains poor. The dual nature (promotion or inhibition) of S100A2 in different cancer types shows the complex involvement of its tumorigenesis, but its effect in ccRCC remains unclear. In this study, we first elucidate the tumor-promoting function of S100A2 in ccRCC by reprogramming glycolysis. Mechanistically, we demonstrate that S100A2 accelerates cancer progression through its interaction with the transcription factor HNF1A, leading to activating GLUT2 transcription. The upregulation of GLUT2 significantly enhances glucose uptake by cancer cells, thereby fueling augmented glucose metabolism and fostering the malignant progression of ccRCC. Collectively, our findings highlight the pivotal role of the S100A2-HNF1A-GLUT2 axis in promoting migration and invasion of ccRCC by amplifying glycolysis and suggest that targeting the S100A2-HNF1A-GLUT2 axis is clinically relevant for the treatment of metastatic ccRCC.
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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.