ArticleCell metabolism2019
Fibroblasts Mobilize Tumor Cell Glycogen to Promote Proliferation and Metastasis.
Article in Cell metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 papers.
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Who cites it
187 citing papers in PubMed, 297 citations in OpenAlex.
- Tumor microenvironment evaluation promotes precise checkpoint immunotherapy of advanced gastric cancer.Journal for immunotherapy of cancer · 2021Trial
- Cancer-Associated Fibroblasts Promote Glucose Metabolic Reprogramming and Progression of Triple-Negative Breast Cancer via Exosomal circFAD104-Mediated Intercellular Communication.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Metabolic buffering restricts phenotype switching in melanoma.The EMBO journal · 2026Article
- Silencing the Signal: The Metastasis Suppressor NDRG1 Disrupts Small Extracellular Vesicle-Mediated Crosstalk in Pancreatic Cancer.Journal of extracellular vesicles · 2026Article
- The lethal symbiont: exploring the pathophysiology of cancer.Physiological reviews · 2026Review
- AKAP1 enhances glycogen accumulation and hepatocarcinogenesis through YTHDF2-mediated G6PC mRNA decay.Signal transduction and targeted therapy · 2026Article
- Glycolytic cancer-associated fibroblasts orchestrate metabolic remodeling in the tumor microenvironment.Journal of experimental & clinical cancer research : CR · 2026Review
- Integrated study reveals molecular mechanisms by which bisphenol A promotes ovarian cancer.iScience · 2026Article
- Single-cell transcriptomic landscape highlights epithelial-fibroblast interactions and CD44-mediated malignant traits in laryngeal squamous cell carcinoma.NPJ precision oncology · 2026Article
- PSMD11 stabilizes PGM3 by antagonizing Parkin to promote bladder cancer progression through energy metabolism reprogramming.Cell death & disease · 2026Article
- Targeting p38α in cancer: challenges, opportunities, and emerging strategies.Molecular oncology · 2026Review
- Current evidence and emerging approaches in immunotherapy for gynecological cancers.Discover oncology · 2026Review
- Absolute dynamic and relative static: the relationship of glycolysis and OXPHOS in cancer development.Cell death discovery · 2026Review
- Molecular and cellular landscapes of the immune microenvironment and multiomic biomarker-sets in platinum-resistant recurrent ovarian cancers.Journal of ovarian research · 2026Review
- Mapping glycogen accumulation and treatment effect in Pompe disease with saturation transfer MRI.Translational research : the journal of laboratory and clinical medicine · 2026Article
- Metabolic reprogramming in cancer: signaling pathways and therapeutic targets.Molecular cancer · 2026Review
- Nanomedicine for targeting cancer-associated fibroblasts in cancer therapy.Theranostics · 2026Review
- Catabolic rewiring in cancer impacts dietary interventions.Communications biology · 2025Review
- Role of metabolic reprogramming of cancer‑associated fibroblasts in tumor development and progression (Review).International journal of oncology · 2025Review
- RNA sequencing and bioinformatics analysis have identifiedTranslational cancer research · 2025Article
127 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 2 countries.
Funding
Abstract
Successful metastasis requires the co-evolution of stromal and cancer cells. We used stable isotope labeling of amino acids in cell culture coupled with quantitative, label-free phosphoproteomics to study the bidirectional signaling in ovarian cancer cells and human-derived, cancer-associated fibroblasts (CAFs) after co-culture. In cancer cells, the interaction with CAFs supported glycogenolysis under normoxic conditions and induced phosphorylation and activation of phosphoglucomutase 1, an enzyme involved in glycogen metabolism. Glycogen was funneled into glycolysis, leading to increased proliferation, invasion, and metastasis of cancer cells co-cultured with human CAFs. Glycogen mobilization in cancer cells was dependent on p38α MAPK activation in CAFs. In vivo, deletion of p38α in CAFs and glycogen phosphorylase inhibition in cancer cells reduced metastasis, suggesting that glycogen is an energy source used by cancer cells to facilitate metastatic tumor growth.
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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.