ReviewCells2018
Elucidating the Metabolic Plasticity of Cancer: Mitochondrial Reprogramming and Hybrid Metabolic States.
Review in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 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
163 citing papers in PubMed.
- MITF-Driven melanoma plasticity as a core mechanism of therapy resistance: integrating microenvironmental signaling, mechanotransduction, and metabolic reprogramming.Cell cycle (Georgetown, Tex.) · 2026Review
- Mechanisms Underlying the Coordination of EMT and Glycolysis Mediated by Hypoxia and Glucose.Current issues in molecular biology · 2026Article
- Article
- Nanocarrier-based delivery of Pt(IV) compounds for chemoimmunotherapy and theranostics: Advances, challenges, and prospects.Acta pharmaceutica Sinica. B · 2026Review
- KRAS Signaling Inhibition Induces a Targetable Metabolic Dependency on Lipophagy-Dependent Fatty Acid Oxidation in Pancreatic Cancer.Cancer research · 2026Article
- Targeting metabolic reprogramming in HPV-associated oral squamous cell carcinoma: current advances, challenges, and clinical prospects.Journal of molecular histology · 2026Review
- Tumor mitochondrial respiration rather than glycolytic activity predicts recurrence in colorectal cancer: an ex vivo bioenergetic profiling study.BMC gastroenterology · 2026Article
- Mitochondrial inhibition enhances the sensitivity of pancreatic ductal adenocarcinoma cells to oncolytic adenovirus.Molecular therapy. Oncology · 2026Article
- Mitochondrial Metabolic Reprogramming in Colorectal Cancer-Associated Fibroblasts: An Up-to-Date Review.Cancers · 2026Review
- Unraveling the nexus in the neuro-neoplastic progression of colorectal cancer: Potential role of β2-adrenergic receptor (β2-AR).Journal of advanced research · 2026Review
- Review
- CGF induces ROS-mediated metabolic reprogramming and mitochondrial dysfunction to suppress colorectal cancer progression.iScience · 2026Article
- Epithelial-Mesenchymal Transition Shapes the Lipotoxic Response of Colon Cancer Cells to Palmitic Acid.Molecular & cellular proteomics : MCP · 2026Article
- Mitochondrial Long Non-Coding RNAs in Gynecological Cancers: Pathogenic Signaling Pathways and Therapeutic Opportunities.Current issues in molecular biology · 2026Review
- Single-Cell Transcriptomic Landscape of Right-Sided Colon Cancer Reveals Cellular and Molecular Features of Metastatic Potential.Biomedicines · 2026Article
- MTP18 as a prognostic biomarker and therapeutic target in lung adenocarcinoma.Respiratory research · 2026Article
- Targeting Dynamin-Related Protein 1 and Glucose Metabolism Reverses Acquired Resistance to Sorafenib in Liver Cancer.Oncology research · 2026Article
- A mechanovascular framework for pre-neoplastic microenvironmental dysregulation and early carcinogenesis.Frontiers in oncology · 2026Article
- Mitochondrial metabolic plasticity in cancer: hybrid bioenergetic states and translational targeting in surgical oncology.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- Herbal Composition Inhibits Mitochondrial Oxidative Phosphorylation to Prevent HER2-Positive Breast Cancer and Identifies Potential Active Compounds.International journal of molecular sciences · 2025Article
103 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Aerobic glycolysis, also referred to as the Warburg effect, has been regarded as the dominant metabolic phenotype in cancer cells for a long time. More recently, it has been shown that mitochondria in most tumors are not defective in their ability to carry out oxidative phosphorylation (OXPHOS). Instead, in highly aggressive cancer cells, mitochondrial energy pathways are reprogrammed to meet the challenges of high energy demand, better utilization of available fuels and macromolecular synthesis for rapid cell division and migration. Mitochondrial energy reprogramming is also involved in the regulation of oncogenic pathways via mitochondria-to-nucleus retrograde signaling and post-translational modification of oncoproteins. In addition, neoplastic mitochondria can engage in crosstalk with the tumor microenvironment. For example, signals from cancer-associated fibroblasts can drive tumor mitochondria to utilize OXPHOS, a process known as the reverse Warburg effect. Emerging evidence shows that cancer cells can acquire a hybrid glycolysis/OXPHOS phenotype in which both glycolysis and OXPHOS can be utilized for energy production and biomass synthesis. The hybrid glycolysis/OXPHOS phenotype facilitates metabolic plasticity of cancer cells and may be specifically associated with metastasis and therapy-resistance. Moreover, cancer cells can switch their metabolism phenotypes in response to external stimuli for better survival. Taking into account the metabolic heterogeneity and plasticity of cancer cells, therapies targeting cancer metabolic dependency in principle can be made more effective.
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