ArticleAnnals of medicine and surgery (2012)2025
Synergistic effects of doxorubicin and coumarin on colorectal cancer cell proliferation and EMT modulation:
Article in Annals of medicine and surgery (2012), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
- Pinostrobin pentanoate as a selective estrogen receptor-Research in pharmaceutical sciences · 2026Article
- Plant- and Algae-Derived Compounds Enhance the Anticancer Activity of Doxorubicin in Colorectal Cancer Cell Lines.Molecules (Basel, Switzerland) · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Colorectal cancer (CRC) ranks as the third most common cancer and the second leading cause of cancer-related deaths globally. Doxorubicin (DOX), an anti-metabolite and anti-cancer agent, has shown promise in CRC treatment, while coumarin, a natural antioxidant, may help slow CRC growth. Although the combination of coumarin and DOX has been studied in other cancer types, its effectiveness in CRC remains unexamined. This study explores the impact of DOX and coumarin, individually and combined, on CRC cell growth and death, specifically focusing on C26 cells Methods: The MTT assay was used to assess cell proliferation, and RT-qPCR was employed to measure the expression of β-catenin, Twist, Cyclin D1, and ZEB-1. Results: Both DOX and coumarin independently inhibited C26 cell growth, and their combination had a synergistic effect. RT-qPCR analysis indicated a reduction in Twist, Cyclin D1, and ZEB-1 expression following combination treatment, suggesting these molecules are involved in the observed anti-cancer effects. Molecular docking revealed that coumarin can target Twist, Cyclin D1, and ZEB-1 at the protein level. Conclusion: Our findings validate the synergistic effect of DOX and coumarin in inhibiting the proliferation of C26 cells and propose the involvement of the Wnt pathway as a downstream mediator in this treatment. Future research is required to confirm the clinical applicability of this combined treatment for CRC and to elucidate its mechanisms within the body.
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