ArticleFrontiers in oncology2025
Curcumin inhibits colorectal cancer progression by targeting PTBP1 and CDK2-mediated pathways.
Article in Frontiers in oncology, 2025. 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 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.
- The anti-migratory effect of curcumin in colorectal cancer involves IKKβ/NF-κB/Snail-mediated EMT inhibition.Translational cancer research · 2026Article
- Therapeutic Potential ofInternational journal of general medicine · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Colorectal cancer (CRC) remains a significant cause of cancer-related mortality worldwide. Curcumin, a natural polyphenol, has shown promise in targeting key cancer pathways, but its precise molecular mechanisms in CRC are not fully understood. This study investigates the anti-cancer mechanisms of curcumin on CRC progression, focusing on PTBP1 and CDK2 as critical regulators. Methods: The expression of PTBP1 was assessed in clinical CRC samples and curcumin-treated cells via PCR and Western blot. Functional assays-including CCK8, colony formation, flow cytometry, Transwell migration/invasion, and apoptosis/autophagy staining-were conducted to evaluate curcumin's effects. CDK2 was identified as a direct target using pull-down, kinase activity, and immunoprecipitation assays. CDK2 knockout models were used to validate curcumin's effects Results: Curcumin markedly downregulated PTBP1 expression, and suppressed CRC cell proliferation, migration, and invasion while promoting apoptosis and autophagy. Mechanistic analysis revealed direct inhibition of CDK2 by curcumin, disrupting the CDK2-c-MYC-PTBP1 regulatory axis. CDK2 knockout mimicked curcumin's effects but reduced the cells' sensitivity to the treatment. Conclusions: This study uncovers a novel mechanism in which curcumin suppresses CRC progression by targeting the CDK2-c-MYC-PTBP1 axis. These findings provide compelling evidence for curcumin's therapeutic potential and support further clinical investigation.
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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.