ArticleeLife2016
Methylglyoxal, a glycolysis side-product, induces Hsp90 glycation and YAP-mediated tumor growth and metastasis.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 90 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
90 citing papers in PubMed, 127 citations in OpenAlex.
- Glyoxalase 1 loss reduces fatty liver but impairs glucose handling in male mice.Physiological reports · 2026Article
- Crosstalk between S-nitrosylation and glycation defines a metabolic vulnerability in liver and renal cancers.Nature communications · 2026Article
- Turning off methylglyoxal stress: an alternative approach to inhibit MDSC expansion and metastasis in triple-negative breast cancer.Journal for immunotherapy of cancer · 2026Article
- Article
- Targeting YAP: mechanistic breakthroughs and therapeutic prospects in reversing organ fibrosis.Molecular and cellular biochemistry · 2026Review
- Utility and Limitations of the Methyl Diaminobenzene-BODIPY Fluorescent Biosensor for Detecting Methylglyoxal in Cells.ACS omega · 2026Article
- Non-Enzymatic MGO-Glycation of SRSF2 Drives RNA Mis-Splicing.Journal of the American Chemical Society · 2026Article
- Sirtuin 2 Regulates Histone Glycation as a Semi-deglycase.Biochemistry · 2026Article
- Glyoxalase 1 is a proadipogenic gene.The Journal of biological chemistry · 2025Article
- Ryanodine receptor 2-mediated calcium leak is associated with increased glyoxalase I in the aging brain.JCI insight · 2025Article
- Protein modifications by advanced glycation end products (AGEs) in human clear cell renal cell carcinoma.Journal of translational medicine · 2025Article
- Energy Metabolism and Brain Aging: Strategies to Delay Neuronal Degeneration.Cellular and molecular neurobiology · 2025Review
- Exploring glycolytic enzymes in disease: potential biomarkers and therapeutic targets in neurodegeneration, cancer and parasitic infections.Open biology · 2025Review
- HSP90 inhibitor AUY922 suppresses tumor growth and modulates immune response through YAP1-TEAD pathway inhibition in gastric cancer.Cancer letters · 2025Article
- Advanced Glycation End-Product-Modified Heat Shock Protein 90 May Be Associated with Urinary Stones.Diseases (Basel, Switzerland) · 2025Article
- Dual roles of methylglyoxal in cancer.Frontiers in oncology · 2025Review
- Metabolic reprogramming and epigenetic effects due to reducing sugars and glycation products in cancer.Frontiers in epigenetics and epigenomics · 2025Review
- Generation and Accumulation of Various Advanced Glycation End-Products in Cardiomyocytes May Induce Cardiovascular Disease.International journal of molecular sciences · 2024Review
- Protein Haptenation and Its Role in Allergy.Chemical research in toxicology · 2024Review
- Review
30 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
25 authors at 7 institutions in 7 countries.
Funding
Abstract
Metabolic reprogramming toward aerobic glycolysis unavoidably induces methylglyoxal (MG) formation in cancer cells. MG mediates the glycation of proteins to form advanced glycation end products (AGEs). We have recently demonstrated that MG-induced AGEs are a common feature of breast cancer. Little is known regarding the impact of MG-mediated carbonyl stress on tumor progression. Breast tumors with MG stress presented with high nuclear YAP, a key transcriptional co-activator regulating tumor growth and invasion. Elevated MG levels resulted in sustained YAP nuclear localization/activity that could be reverted using Carnosine, a scavenger for MG. MG treatment affected Hsp90 chaperone activity and decreased its binding to LATS1, a key kinase of the Hippo pathway. Cancer cells with high MG stress showed enhanced growth and metastatic potential in vivo. These findings reinforce the cumulative evidence pointing to hyperglycemia as a risk factor for cancer incidence and bring renewed interest in MG scavengers for cancer treatment.
Indexed as
Identifiers
What OpenQuestion holds
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.