ArticleCurrent medical science2025
NOX4 Suppresses Ferroptosis Through Regulation of the Pentose Phosphate Pathway in Colorectal Cancer.
Article in Current medical science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Artificial-intelligence- and multi-omics-guided predictive and drug repurposing framework construction for colorectal cancer: evidence from succinylation-neutrophil signatures.Frontiers in cell and developmental biology · 2026Article
- Glucose Metabolic Reprogramming in Colorectal Cancer: From Mechanisms to Targeted Therapy Approaches.Cancer medicine · 2025Review
- Identification of ferroptosis related genes and subtypes in colorectal cancer.Scientific reports · 2025Article
- Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveNicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) are known as major sources of reactive oxygen species (ROS), yet their role in regulating cellular antioxidative metabolism and ferroptosis is unclear. This study assessed the expression and clinical relevance of NOXs across pan-cancer and investigated the role of NOX4 in colorectal cancer progression
methodsWe analyzed transcriptomic and survival data from The Cancer Genome Atlas (TCGA) for NOXs across 22 types of solid tumors. A CRISPR library targeting NOXs was developed for potential therapeutic target screening in colorectal cancer cells (CRCs). Techniques such as CRISPR-knockout cell lines, 1,2-
resultsNOX4 emerged as a key therapeutic target for colorectal cancer from TCGA data. CRISPR screening highlighted its essential role in CRC survival, with functional experiments confirming that NOX4 upregulation promotes cell survival and proliferation. The interaction of NOX4 with glucose‑6‑phosphate dehydrogenase (G6PD) was found to enhance the pentose phosphate pathway (PPP), facilitating ROS clearance and protecting CRCs against ferroptosis.
conclusionsThis study identified NOX4 as a novel ferroptosis suppressor and a therapeutic target for the treatment of colorectal cancer. The findings suggest that a coupling between NADPH oxidase enzyme NOX4 and the PPP regulates ferroptosis and reveal an accompanying metabolic vulnerability for therapeutic targeting in colorectal cancer.
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