ArticleApoptosis : an international journal on programmed cell death2025
Aspirin-Inspired 6-O-Carboxymethyl-N-Acetylglucosamine: A potent antitumor agent with enhanced efficacy.
Article in Apoptosis : an international journal on programmed cell death, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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.
- Bioactive Chitin-Based Thermosensitive Hydrogel Reinforces Stem Cell Therapy for Osteoarthritis.Biomaterials research · 2026Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Aspirin, widely recognized for its anti-inflammatory and cardioprotective effects, has also shown potential as a cancer therapeutic. However, its clinical application is hindered by severe adverse effects. Here, we explore 6-O-Carboxymethyl-N-Acetylglucosamine (CM-NAG) a novel derivative of N-acetylglucosamine, designed to mimic the structural and functional properties of aspirin. CM-NAG significantly inhibits the viability of both colorectal and pancreatic cancer cells. In colorectal cancer cells, CM-NAG also suppressed migration and invasion and induced apoptosis more effectively than aspirin. Mechanistically, CM-NAG upregulated phosphoenolpyruvate carboxykinase 2 (PCK2), a key regulator of gluconeogenesis in colorectal cancer cells. In a xenograft model, CM-NAG reduced tumor size and improved histopathological outcomes, while showing no significant toxicity in major organs. The expression of PCK2 in CRC tissues was significantly lower than in cancer-adjacent tissues, according immunohistochemistry analysis. Clinical analysis revealed high PCK2 expression in colorectal cancer tissues correlates with better disease-free survival, supporting PCK2 as a promising therapeutic target. These findings suggest that CM-NAG may represent a next-generation antitumor agent with enhanced efficacy and safety compared to aspirin, offering new prospects for cancer treatment.
Indexed as
Identifiers
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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.