ArticleCancer cell international2026
Silencing Uracil-DNA glycosylase inhibits colorectal cancer progression.
Article in Cancer cell international, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
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
1 citing paper in PubMed.
- Correction: Silencing Uracil-DNA glycosylase inhibits colorectal cancer progression.Cancer cell international · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
Abstract
Dysregulation of repair pathways, specifically the base excision repair (BER) axis, is frequently observed in cancer. This dysfunction is associated with accelerated tumor growth and reduced patient survival, suggesting that BER components may serve as potential targets for cancer therapy. This study focused on the expression of Uracil-DNA glycosylase (UNG), a key enzyme in BER, in colorectal tumor tissues and adjacent normal tissues. We systematically explored the clinical significance, biological functions, and molecular mechanisms of UNG in colorectal cancer (CRC). Our findings revealed that UNG was significantly upregulated in CRC, and its higher expression correlated with poorer patient outcomes. Functional assays demonstrated that silencing UNG inhibited cell proliferation, reduced migration and invasion capabilities, and induced apoptosis along with S/G2 phase cell cycle arrest. Mechanistically, UNG appears to interact with the AMPK, AKT/mTOR, and ERK signaling pathways. These results suggested that UNG exhibited oncogenic potential in CRC by regulating malignant behaviors and oncogenic signaling cascades, positioned it as a potential prognostic biomarker and therapeutic target for CRC treatment.
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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 Socratic graph.