ArticleDiscover oncology2025
HADHB mediates 5-fluorouracil sensitivity in colorectal cancer.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
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
2 citing papers in PubMed.
- Recent Advances and Future Directions in 5-Fluorouracil Drug Delivery: A Comprehensive Review.Current topics in medicinal chemistry · 2026Review
- Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
purpose5-Fluorouracil (5FU) is a primary chemotherapy for colorectal cancer (CRC), but resistance reduces its effectiveness. HADHB, important in mitochondrial fatty acid β-oxidation, is linked to tumor metabolism changes in various cancers. Its potential influence on 5FU sensitivity in CRC remains unclear. This study aims to elucidate the role of HADHB in modulating 5FU sensitivity in CRC.
methodsCollect CRC tissue samples treated with 5FU and perform immunohistochemical staining to evaluate the relationship between HADHB expression and 5FU efficacy. We assessed the impact of HADHB on 5FU IC
resultsHADHB was significantly upregulated in 5FU-resistant CRC tissues compared to sensitive ones. HADHB knockdown in CRC cell lines improved 5FU sensitivity, increased apoptosis, and caused cell cycle arrest. We identified DUOX2 as a novel HADHB-interacting protein, with their protein levels showing strong positive correlation. Silencing either HADHB or DUOX2 can result in a decrease in ROS production, while DUOX2 overexpression reversed the ROS reduction caused by HADHB knockdown, thereby establishing a functional connection between these two elements in the regulation of ROS. This mechanism may play a crucial role in modulating the sensitivity to 5FU mediated by HADHB.
conclusionHADHB overexpression is linked to 5FU resistance in CRC, indicating it as a potential therapeutic target, likely via the HADHB-DUOX2-ROS pathway.
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Registered trials
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