ArticleClinical and translational medicine2022
Nicotinamide-N-methyltransferase is a promising metabolic drug target for primary and metastatic clear cell renal cell carcinoma.
Article in Clinical and translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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27 citing papers in PubMed, 37 citations in OpenAlex.
- Triggering SORL1 Expression Restricts ccRCC Progression by Inducing Ubiquitination-Mediated c-Myc Degradation.Cancer science · 2026Article
- NNMT and the methylation sink: integrating metabolism, epigenetics and immunity in cancer.BMC medicine · 2026Review
- From Genes to Proteins: The Indispensable Role of Proteogenomics in Advancing Clear Cell Renal Cell Carcinoma Research.International journal of molecular sciences · 2026Review
- A non-complement role for C1R rewires integrin and death-receptor signaling to drive renal cancer metastasis.Molecular cancer · 2026Article
- Identification of shared diagnostic biomarkers and molecular pathways between chronic kidney disease and renal cell carcinoma using transcriptomics and machine learning.Translational cancer research · 2026Article
- Article
- Computational assessment of the relationship between metabolism and histone methylation in cancer cells.PloS one · 2026Article
- Prognostic and Therapeutic Potential of Nicotinamide N-Methyltransferase and Hypoxia Inducible Lipid Droplet Associated in Clear Cell Renal Cell Carcinoma.Journal of Korean medical science · 2025Article
- Renal cell carcinoma organoids for precision medicine: bridging the gap between models and patients.Journal of translational medicine · 2025Review
- Single-cell sequencing technology in renal cancer: insights into tumor biology and clinical application.Biomarker research · 2025Review
- Nicotinamide N-methyltransferase enhances paclitaxel resistance in ovarian clear cell carcinoma.Human cell · 2025Article
- Replacing normalizations with interval assumptions enhances differential expression and differential abundance analyses.BMC bioinformatics · 2025Article
- Nicotinamide N-Methyltransferase in the Inflammatory Pathogenesis of Graves' Orbitopathy.Investigative ophthalmology & visual science · 2025Article
- Heterogeneous and novel transcript expression in single cells of patient-derived clear cell renal cell carcinoma organoids.Genome research · 2025Article
- m6Am Methyltransferase PCIF1 Promotes LPP3 Mediated Phosphatidic Acid Metabolism and Renal Cell Carcinoma Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The Use of Patient-Derived Organoids in the Study of Molecular Metabolic Adaptation in Breast Cancer.International journal of molecular sciences · 2024Review
- Elevated Plasma Concentration of 4-Pyridone-3-carboxamide-1-β-D-ribonucleoside (4PYR) Highlights Malignancy of Renal Cell Carcinoma.International journal of molecular sciences · 2024Article
- The Role of NADPharmaceuticals (Basel, Switzerland) · 2024Review
- It Takes Two to Tango: The Interplay between Prostate Cancer and Its Microenvironment from an Epigenetic Perspective.Cancers · 2024Review
- A pilot radiometabolomics integration study for the characterization of renal oncocytic neoplasia.Scientific reports · 2023Article
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Authors and funding
19 authors at 6 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundThe metabolic enzyme nicotinamide-N-methyltransferase (NNMT) is highly expressed in various cancer entities, suggesting tumour-promoting functions. We systematically investigated NNMT expression and its metabolic interactions in clear cell renal cell carcinoma (ccRCC), a prominent RCC subtype with metabolic alterations, to elucidate its role as a drug target.
methodsNNMT expression was assessed in primary ccRCC (n = 134), non-tumour tissue and ccRCC-derived metastases (n = 145) by microarray analysis and/or immunohistochemistry. Findings were validated in The Cancer Genome Atlas (kidney renal clear cell carcinoma [KIRC], n = 452) and by single-cell analysis. Expression was correlated with clinicopathological data and survival. Metabolic alterations in NNMT-depleted cells were assessed by nontargeted/targeted metabolomics and extracellular flux analysis. The NNMT inhibitor (NNMTi) alone and in combination with the inhibitor 2-deoxy-D-glucose for glycolysis and BPTES (bis-2-(5-phenylacetamido-1,3,4-thiadiazol-2-yl)ethyl-sulfide) for glutamine metabolism was investigated in RCC cell lines (786-O, A498) and in two 2D ccRCC-derived primary cultures and three 3D ccRCC air-liquid interface models.
resultsNNMT protein was overexpressed in primary ccRCC (p = 1.32 × 10
conclusionsSince efficient glutamine utilisation, which is essential for ccRCC tumours, depends on NNMT, small-molecule NNMT inhibitors provide a novel therapeutic strategy for ccRCC and act as sensitizers for combination therapies.
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