ArticleiScience2025
Multilevel plasticity and altered glycosylation drive aggressiveness in hypoxic and glucose-deprived bladder cancer cells.
Article in iScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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
8 citing papers in PubMed.
- CD276 immature glycosylation drives colorectal cancer aggressiveness and T cell mediated immune escape.Cell communication and signaling : CCS · 2026Article
- Short-term hypoxia and nutrient deprivation stress induced shifts in p53 isoform expression in HepG2 tumourspheres.Molecular biology reports · 2026Article
- O-glycosylation in Cancer: Emerging Paradigms and Prospects for Precision Oncology.International journal of biological sciences · 2026Review
- Adhesion to aggression: unravelling sLeClinical & experimental metastasis · 2025Review
- Glycomics and Glycoproteomics Reveal Distinct Oligomannose Carriers Across Bladder Cancer Stages.International journal of molecular sciences · 2025Article
- E-selectin affinity glycoproteomics reveals neuroendocrine proteins and the secretin receptor as a poor-prognosis signature in colorectal cancer.Molecular oncology · 2025Article
- Stool Glycoproteomics Signatures of Pre-Cancerous Lesions and Colorectal Cancer.International journal of molecular sciences · 2024Article
- Aberrantly Glycosylated GLUT1 as a Poor Prognosis Marker in Aggressive Bladder Cancer.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
22 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bladder tumors with aggressive characteristics often present microenvironmental niches marked by low oxygen levels (hypoxia) and limited glucose supply due to inadequate vascularization. The molecular mechanisms facilitating cellular adaptation to these stimuli remain largely elusive. Employing a multi-omics approach, we discovered that hypoxic and glucose-deprived cancer cells enter a quiescent state supported by mitophagy, fatty acid β-oxidation, and amino acid catabolism, concurrently enhancing their invasive capabilities. Reoxygenation and glucose restoration efficiently reversed cell quiescence without affecting cellular viability, highlighting significant molecular plasticity in adapting to microenvironmental challenges. Furthermore, cancer cells exhibited substantial perturbation of protein
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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.