ArticleMetabolic engineering2022
Elucidating tumor-stromal metabolic crosstalk in colorectal cancer through integration of constraint-based models and LC-MS metabolomics.
Article in Metabolic engineering, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- IRS2 as a driver and therapeutic target in brain metastases from colorectal cancer: a systematic review of mechanistic and translational evidence.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Pooled it
- Bioengineered systems to exploit tumor microenvironment metabolism.Trends in cancer · 2026Review
- Decoding the CAF-TAM axis: multi-omics dissection and therapeutic targeting of stromal-immune crosstalk in the tumor microenvironment.Cell death & disease · 2026Review
- Cancer-associated fibroblasts drive metabolic heterogeneity in colorectal cancer cells: predictions from metabolic modeling.NPJ systems biology and applications · 2026Article
- Gut microbiota characteristics of gastric cancer patients across distinct pathological stages and their associations with tumor and paratumor mucosal microbiota.Frontiers in cellular and infection microbiology · 2026Article
- Crosstalk between mFrontiers in immunology · 2026Review
- Merging metabolic modeling and imaging for screening therapeutic targets in colorectal cancer.NPJ systems biology and applications · 2025Article
- Merging Metabolic Modeling and Imaging for Screening Therapeutic Targets in Colorectal Cancer.bioRxiv : the preprint server for biology · 2024Article
- Advances in targeting cancer-associated fibroblasts through single-cell spatial transcriptomic sequencing.Biomarker research · 2024Review
- Peptide set test: a peptide-centric strategy to infer differentially expressed proteins.Bioinformatics (Oxford, England) · 2024Article
- Flux sampling in genome-scale metabolic modeling of microbial communities.BMC bioinformatics · 2024Article
- Define cancer-associated fibroblasts (CAFs) in the tumor microenvironment: new opportunities in cancer immunotherapy and advances in clinical trials.Molecular cancer · 2023Review
- Genome-scale modeling predicts metabolic differences between macrophage subtypes in colorectal cancer.iScience · 2023Article
- Flux Sampling in Genome-scale Metabolic Modeling of Microbial Communities.bioRxiv : the preprint server for biology · 2023Article
- Ensemble-based genome-scale modeling predicts metabolic differences between macrophage subtypes in colorectal cancer.bioRxiv : the preprint server for biology · 2023Article
- Warburg effect in colorectal cancer: the emerging roles in tumor microenvironment and therapeutic implications.Journal of hematology & oncology · 2022Review
- Resource allocation in mammalian systems.Biotechnology advancesReview
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Colorectal cancer (CRC) is a major cause of morbidity and mortality in the United States. Tumor-stromal metabolic crosstalk in the tumor microenvironment promotes CRC development and progression, but exactly how stromal cells, in particular cancer-associated fibroblasts (CAFs), affect the metabolism of tumor cells remains unknown. Here we take a data-driven approach to investigate the metabolic interactions between CRC cells and CAFs, integrating constraint-based modeling and metabolomic profiling. Using metabolomics data, we perform unsteady-state parsimonious flux balance analysis to infer flux distributions for central carbon metabolism in CRC cells treated with or without CAF-conditioned media. We find that CAFs reprogram CRC metabolism through stimulation of glycolysis, the oxidative arm of the pentose phosphate pathway (PPP), and glutaminolysis, as well as inhibition of the tricarboxylic acid cycle. To identify potential therapeutic targets, we simulate enzyme knockouts and find that CAF-treated CRC cells are especially sensitive to inhibitions of hexokinase and glucose-6-phosphate, the rate limiting steps of glycolysis and oxidative PPP. Our work gives mechanistic insights into the metabolic interactions between CRC cells and CAFs and provides a framework for testing hypotheses towards CRC-targeted therapies.
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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.