ArticleCancer research2017
Modeling the Genetic Regulation of Cancer Metabolism: Interplay between Glycolysis and Oxidative Phosphorylation.
Article in Cancer research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 papers, 1 of them a synthesis that pooled it.
What it found
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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
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Who cites it
187 citing papers in PubMed, 1 synthesis or guideline pooled it, 280 citations in OpenAlex.
- PD-L1 Activity Is Associated with Partial EMT and Metabolic Reprogramming in Carcinomas.Current oncology (Toronto, Ont.) · 2022Pooled it
- Truncating the time-evolving discrete chemical master equation for stochastic biological networks.Biophysical journal · 2026Article
- A State-Gated Metallo-DNAzyme Framework Programs Tumor Stress Vulnerability Through Metabolic Licensing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Mechanisms Underlying the Coordination of EMT and Glycolysis Mediated by Hypoxia and Glucose.Current issues in molecular biology · 2026Article
- Adaptive epithelial-mesenchymal bi-directional transition: A key invasive plasticity for tumor metastasis.iScience · 2026Review
- Age-Associated NAD+ Decline and Mitochondrial Dysfunction Predispose Cells to a Reversible Tumor-Permissive Metabolic State.Biology · 2026Article
- Mitochondrial inhibition enhances the sensitivity of pancreatic ductal adenocarcinoma cells to oncolytic adenovirus.Molecular therapy. Oncology · 2026Article
- Metab8D: a metabolic regulome network from multiomics and machine learning.Communications biology · 2026Article
- Cellular mechanometabolism: stimuli and implications.EMBO reports · 2026Review
- Hallmarks of epithelial-mesenchymal plasticity in cancer.Molecular cancer · 2026Review
- Decoding the metabolic cipher of dormant cancer cells: molecular mechanisms and therapeutic potentials.Cell communication and signaling : CCS · 2026Review
- Vitamin B3 suppressesTranslational cancer research · 2026Article
- Dual targeting of PI3Kδ and PPARα enhances antitumor activity via FoxO1 activation in follicular lymphoma.Cell death & disease · 2026Article
- Absolute dynamic and relative static: the relationship of glycolysis and OXPHOS in cancer development.Cell death discovery · 2026Review
- Single-Cell Transcriptomic Landscape of Right-Sided Colon Cancer Reveals Cellular and Molecular Features of Metastatic Potential.Biomedicines · 2026Article
- Ophiobolin A impacts mitochondrial redox biology in an epithelial-mesenchymal transition (EMT)-specific manner.Cancer cell international · 2026Article
- Mitochondrial metabolic plasticity in cancer: hybrid bioenergetic states and translational targeting in surgical oncology.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- Dynamic Metabolic States in TNBC: Orchestrating Spatiotemporal Adaptation and Therapy.Oncology research · 2026Review
- Dual Metabolic Inhibition by Berberine and Glutor Triggers AMPK/JNK-Dependent DNA Damage in Cancer Cells.International journal of medical sciences · 2026Article
- Mitochondrial metabolic-transcriptional axis drives adaptive drug tolerance across major lung cancer subtypes.Frontiers in genetics · 2026Review
127 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
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Abnormal metabolism is a hallmark of cancer, yet its regulation remains poorly understood. Cancer cells were considered to utilize primarily glycolysis for ATP production, referred to as the Warburg effect. However, recent evidence suggests that oxidative phosphorylation (OXPHOS) plays a crucial role during cancer progression. Here we utilized a systems biology approach to decipher the regulatory principle of glycolysis and OXPHOS. Integrating information from literature, we constructed a regulatory network of genes and metabolites, from which we extracted a core circuit containing HIF-1, AMPK, and ROS. Our circuit analysis showed that while normal cells have an oxidative state and a glycolytic state, cancer cells can access a hybrid state with both metabolic modes coexisting. This was due to higher ROS production and/or oncogene activation, such as RAS, MYC, and c-SRC. Guided by the model, we developed two signatures consisting of AMPK and HIF-1 downstream genes, respectively, to quantify the activity of glycolysis and OXPHOS. By applying the AMPK and HIF-1 signatures to The Cancer Genome Atlas patient transcriptomics data of multiple cancer types and single-cell RNA-seq data of lung adenocarcinoma, we confirmed an anticorrelation between AMPK and HIF-1 activities and the association of metabolic states with oncogenes. We propose that the hybrid phenotype contributes to metabolic plasticity, allowing cancer cells to adapt to various microenvironments. Using model simulations, our theoretical framework of metabolism can serve as a platform to decode cancer metabolic plasticity and design cancer therapies targeting metabolism.
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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.