ArticleCell death and differentiation2025
Cancer-intrinsic Cxcl5 orchestrates a global metabolic reprogramming for resistance to oxidative cell death in 3D.
Article in Cell death and differentiation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Who cites it
3 citing papers in PubMed.
- Cuproptosis and ferroptosis: signal pathways, diseases and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Ferroptosis in cancer toward molecular insights and clinical translation in pancreatic cancer.Molecular cancer · 2026Review
- Sucrose fuels liver cancer cell growth and spheroid formation: New insights from 2D and 3D cell culture models.Medicine internationalArticle
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Pancreatic ductal adenocarcinoma is characterized by a three-dimensional (3D) tumor microenvironment devoid of oxygen and nutrients but enriched in extracellular matrix, which acts as a physical and chemical barrier. In 3D, cancer cells reprogram their metabolic pathways in ways that help them survive hostile conditions. However, little is known about the metabolic phenotypes of cancer cells in 3D and the intrinsic cues that modulate them. We found that Cxcl5 deletion restricted pancreatic tumor growth in a 3D spheroid-in-Matrigel culture system without affecting cancer cell growth in 2D culture. Cxcl5 deletion impaired 3D-specific global metabolic reprogramming, resistance to hypoxia-induced cell death, and upregulation of Hif1α and Myc. Overexpression of Hif1α and Myc, however, effectively restored 3D culture-induced metabolic reconfiguration, growth, redox homeostasis, and mitochondrial function in Cxcl5
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