ArticlePloS one2019
Breast cancers utilize hypoxic glycogen stores via PYGB, the brain isoform of glycogen phosphorylase, to promote metastatic phenotypes.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Brain-Type Glycogen Phosphorylase (PYGB) in the Pathologies of Diseases: A Systematic Review.Cells · 2024Pooled it
- Modulation of the tumor microenvironment through BMAL1-LHX8 axis augments the sensitivity of ameloblastoma to vemurafenib.Journal of advanced research · 2026Article
- Metabolic buffering restricts phenotype switching in melanoma.The EMBO journal · 2026Article
- Hypoxia Signaling and Non-Coding RNAs: Regulatory Networks and Therapeutic Implications in Breast Cancer.Current issues in molecular biology · 2026Review
- Metabolic reprogramming and interventions in angiogenesis.Journal of advanced research · 2025Review
- TMT-Based Quantitative Proteomic Profiling of Human Esophageal Cancer Cells Reveals the Potential Mechanism and Potential Therapeutic Targets Associated With Radioresistance.Proteomics. Clinical applications · 2025Article
- Comprehensive single-cell aging atlas of healthy mammary tissues reveals shared epigenomic and transcriptomic signatures of aging and cancer.Nature aging · 2025Article
- An 11-gene glycosyltransferases-related model for the prognosis of patients with bladder urothelial carcinoma: development and validation based on TCGA and GEO datasets.Translational andrology and urology · 2024Article
- Ubiquitin-related gene markers predict immunotherapy response and prognosis in patients with epithelial ovarian carcinoma.Scientific reports · 2024Article
- Glucose metabolism in B cell malignancies: a focus on glycolysis branching pathways.Molecular oncology · 2024Review
- Cancer Metabolism under Limiting Oxygen Conditions.Cold Spring Harbor perspectives in medicine · 2024Review
- Breast cancer cells and adipocytes in hypoxia: metabolism regulation.Discover oncology · 2024Review
- Comprehensive single cell aging atlas of mammary tissues reveals shared epigenomic and transcriptomic signatures of aging and cancer.bioRxiv : the preprint server for biology · 2023Article
- Glycogen synthase 1 targeting reveals a metabolic vulnerability in triple-negative breast cancer.Journal of experimental & clinical cancer research : CR · 2023Article
- PYGL-mediated glucose metabolism reprogramming promotes EMT phenotype and metastasis of pancreatic cancer.International journal of biological sciences · 2023Article
- Inhibition of Glycogen Metabolism Induces Reactive Oxygen Species-Dependent Cytotoxicity in Anaplastic Thyroid Cancer in Female Mice.Endocrinology · 2022Article
- Analysis of the expression, function and signaling of glycogen phosphorylase isoforms in hepatocellular carcinoma.Oncology letters · 2022Article
- A Proteomic Platform Unveils the Brain Glycogen Phosphorylase as a Potential Therapeutic Target for Glioblastoma Multiforme.International journal of molecular sciences · 2022Article
- Liver glycogen phosphorylase is upregulated in glioblastoma and provides a metabolic vulnerability to high dose radiation.Cell death & disease · 2022Article
- Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
In breast cancer, tumor hypoxia has been linked to poor prognosis and increased metastasis. Hypoxia activates transcriptional programs in cancer cells that lead to increased motility and invasion, as well as various metabolic changes. One of these metabolic changes, an increase in glycogen metabolism, has been further associated with protection from reactive oxygen species damage that may lead to premature senescence. Here we report that breast cancer cells significantly increase glycogen stores in response to hypoxia. We found that knockdown of the brain isoform of an enzyme that catalyzes glycogen breakdown, glycogen phosphorylase B (PYGB), but not the liver isoform, PYGL, inhibited glycogen utilization in estrogen receptor negative and positive breast cancer cells; whereas both independently inhibited glycogen utilization in the normal-like breast epithelial cell line MCF-10A. Functionally, PYGB knockdown and the resulting inhibition of glycogen utilization resulted in significantly decreased wound-healing capability in MCF-7 cells and a decrease in invasive potential of MDA-MB-231 cells. Thus, we identify PYGB as a novel metabolic target with potential applications in the management and/or prevention of metastasis in breast cancer.
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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.