ArticlePloS one2024
SLC2A3 promotes tumor progression through lactic acid-promoted TGF-β signaling pathway in oral squamous cell carcinoma.
Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 6 citations in OpenAlex.
- Mechanisms Underlying the Coordination of EMT and Glycolysis Mediated by Hypoxia and Glucose.Current issues in molecular biology · 2026Article
- METTL3-catalyzed m6A modification of NSUN4 mediates m5C modification of SLC2A3 mRNA to regulate PDGF-BB-induced proliferation, hyaluronan production and glycolysis in human orbital fibroblasts.Journal of bioenergetics and biomembranes · 2026Article
- Exosomes from tumor-associated macrophages promote glycolysis and malignant NSCLC progression by delivery of hsa_circ_0000896.Biology direct · 2026Article
- Silencing THBS1 in M2 Macrophages Exerts an Inhibitory Effect on Tongue Squamous Cell Carcinoma by Suppressing TGF-β Pathway.Biochemical genetics · 2026Article
- SLC2A3-Mediated Lactate Metabolism Promotes Lung Cancer Bone Metastasis by Modulating P53 Lactylation and Immune Evasion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Possibility of Plasma Membrane Transporters as Drug Targets in Oral Cancers.International journal of molecular sciences · 2025Review
- TAGLN-RhoA/ROCK2-SLC2A3-mediated Mechano-metabolic Axis Promotes Skin Fibrosis.International journal of biological sciences · 2025Article
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3 authors at 1 institution in 1 country.
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Abstract
backgroundsOral squamous cell carcinoma is a malignant tumor of the head and neck, and its molecular mechanism remains to be explored.
methodsBy analyzing the OSCC data from the TCGA database, we found that SLC2A3 is highly expressed in OSCC patients. The expression level of SLC2A3 was verified by RT-PCR and western blotting in OSCC cell lines. The function of SLC2A3 in OSCC cell lines and Lactic acid in SLC2A3-knockdown OSCC cells were detected by colony formation, CCK8, transwell, and wound healing assays. The effect of SLC2A3 on tumor growth and metastasis was tested in vivo. GSEA and Western blot were used to analyze and validate tumor phenotypes and signaling pathway molecules.
resultsWe analyzed OSCC datasets in the TCGA database and found that SLC2A3 had abnormally high expression and was associated with poor prognosis. We also found that oral squamous cell carcinoma cells had increased proliferation, migration, invasion, EMT phenotype, and glycolysis due to SLC2A3 overexpression. Conversely, SLC2A3 knockdown had the opposite effect. Our in vivo experiments confirmed that SLC2A3 overexpression promoted tumor growth and metastasis while knockdown inhibited it. We also observed that high SLC2A3 expression led to EMT and the activation of the TGF-β signaling pathway, while knockdown inhibited it. Interestingly, exogenous lactic acid restored the EMT, proliferation, migration, and invasion abilities of oral cancer cells inhibited by knocking down SLC2A3.
conclusionsOur study reveals that SLC2A3 expression was up-regulated in OSCC. SLC2A3 activates the TGF-β signaling pathway through lactic acid generated from glycolysis, thus regulating the biological behavior of OSCC.
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