ArticleJournal of cell science2025
The STEAP4 target NQO1 mediates colon tumorigenesis.
Article in Journal of cell science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Article
- Iron Metabolism in the Colorectal Tumor Microenvironment: Current Evidence and Clinical Implications.Diagnostics (Basel, Switzerland) · 2026Review
- Iron Metabolism in the Colorectal Tumor Microenvironment: From Preneoplastic Lesions to Cancer Progression.International journal of molecular sciences · 2026Review
- Ferritinophagy Loss Drives Mitochondrial Iron Import and Colorectal Tumorigenesis.Research square · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Colorectal cancer (CRC) remains a major global health concern, necessitating advancements in therapeutic strategies. Understanding the mechanisms driving CRC is crucial for developing effective treatments. Previous studies, including our own, highlight the role of six-transmembrane epithelial antigen of prostate 4 (STEAP4) in promoting colon tumorigenesis through reactive oxygen species (ROS) generation, making it a promising target. Our research provides compelling evidence that STEAP4 knockout significantly reduces colon tumorigenesis in a genetically engineered mouse model. Suppressing STEAP4 via knockdown techniques effectively attenuated the nuclear factor erythroid 2-related factor 2 (NRF2)-NAD(P)H:quinone oxidoreductase 1 (NQO1) signaling pathway, inducing apoptosis and autophagy, leading to substantial reductions in xenograft tumor growth. In contrast, STEAP4 overexpression amplified ROS production and activated the NRF2-NQO1 pathway in a ferric iron (Fe3+)-dependent manner. Notably, bioactivatable drugs targeting NQO1 were highly effective at eradicating STEAP4-overexpressing colon cancer cells. These findings highlight the potential of targeted therapeutic interventions for CRC, particularly through STEAP4 modulation. In conclusion, our study advances understanding of the role of STEAP4 in colon tumorigenesis, offering promising avenues for novel CRC treatments.
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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.