ReviewCells2019
Metabolic Dysregulations and Epigenetics: A Bidirectional Interplay that Drives Tumor Progression.
Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 62 citations in OpenAlex.
- Systemic epigenetic dysregulation as a driver of ageing and a therapeutic target.Nature reviews. Molecular cell biology · 2026Review
- Therapeutic implications of epigenetic alterations in burns: a new frontier in burn medicine.Clinical science (London, England : 1979) · 2026Review
- Role and clinical importance of lactylation in tumors (Review).Molecular medicine reports · 2026Review
- BPGM shapes NFAT5-driven cellular responses.Cellular and molecular life sciences : CMLS · 2026Article
- Review
- Epigenomic and Metabolic Interplay in the Development of Metastatic Brain Tumors.Oncology research · 2026Review
- Review
- From Data to Cure: A Comprehensive Exploration of Multi-omics Data Analysis for Targeted Therapies.Molecular biotechnology · 2025Review
- Metabolomics as the missing piece in epigenetics research.Environmental epigenetics · 2025Article
- Inhibition of Mettl3 alleviates low-dose cisplatin-induced renal fibrosis and enhances the chemotherapeutic efficacy in mouse models of cancer.International journal of biological sciences · 2025Article
- Revolutionizing Cancer Treatment: Harnessing the Power of Mesenchymal Stem Cells for Precise Targeted Therapy in the Tumor Microenvironment.Current topics in medicinal chemistry · 2025Review
- Epigenetic regulation of transcription factors involved in NLRP3 inflammasome and NF-kB signaling pathways.Frontiers in immunology · 2025Review
- Role of Fatty Acids β-Oxidation in the Metabolic Interactions Between Organs.International journal of molecular sciences · 2024Review
- Nuclear localization of MTHFD2 is required for correct mitosis progression.Nature communications · 2024Article
- TRAP1 modulates mitochondrial biogenesis via PGC-1α/TFAM signalling pathway in colorectal cancer cells.Journal of molecular medicine (Berlin, Germany) · 2024Article
- A prismatic view of the epigenetic-metabolic regulatory axis in breast cancer therapy resistance.Oncogene · 2024Review
- Crosstalk between DNA Damage Repair and Metabolic Regulation in Hematopoietic Stem Cells.Cells · 2024Review
- Nano-energy interference: A novel strategy for blunting tumor adaptation and metastasis.Materials today. Bio · 2024Article
- MTHFD2 in healthy and cancer cells: Canonical and non-canonical functions.npj metabolic health and disease · 2024Review
- AGXT2 Suppresses the Proliferation and Dissemination of Hepatocellular Carcinoma Cells by Modulating Intracellular Lipid Metabolism.Journal of hepatocellular carcinoma · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer has been considered, for a long time, a genetic disease where mutations in keyregulatory genes drive tumor initiation, growth, metastasis, and drug resistance. Instead, theadvent of high-throughput technologies has revolutionized cancer research, allowing to investigatemolecular alterations at multiple levels, including genome, epigenome, transcriptome, proteome,and metabolome and showing the multifaceted aspects of this disease. The multi-omics approachesrevealed an intricate molecular landscape where different cellular functions are interconnected andcooperatively contribute to shaping the malignant phenotype. Recent evidence has brought to lighthow metabolism and epigenetics are highly intertwined, and their aberrant crosstalk can contributeto tumorigenesis. The oncogene-driven metabolic plasticity of tumor cells supports the energeticand anabolic demands of proliferative tumor programs and secondary can alter the epigeneticlandscape via modulating the production and/or the activity of epigenetic metabolites. Conversely,epigenetic mechanisms can regulate the expression of metabolic genes, thereby altering themetabolome, eliciting adaptive responses to rapidly changing environmental conditions, andsustaining malignant cell survival and progression in hostile niches. Thus, cancer cells takeadvantage of the epigenetics-metabolism crosstalk to acquire aggressive traits, promote cellproliferation, metastasis, and pluripotency, and shape tumor microenvironment. Understandingthis bidirectional relationship is crucial to identify potential novel molecular targets for theimplementation of robust anti-cancer therapeutic strategies.
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What OpenQuestion holds
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.