ArticlePhytomedicine : international journal of phytotherapy and phytopharmacology2024
The anticancer effects of Aronia berry extract are mediated by Chk1 and p53 in colorectal cancer.
Article in Phytomedicine : international journal of phytotherapy and phytopharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- An herbal formula, SH003 alleviates colorectal cancer through dual targeting of adaptive and innate checkpoints PD-L1/CD47.Cancer cell international · 2026Article
- A Review ofFoods (Basel, Switzerland) · 2026Review
- Aronia Berry Extract Inhibits Cancer Stemness and Overcomes 5-Fluorouracil Resistance by Targeting TLR3/NF-κB Signaling in Colorectal Cancer.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Checkpoint kinase 1 in colorectal cancer: Upregulation of expression and promotion of cell proliferation.World journal of clinical oncology · 2025Article
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5 authors.
Funding
Abstract
backgroundAronia berry extracts (ABE) have recently been reported to possess significant anti-cancer effects in various malignancies, including colorectal cancer (CRC), due to their high polyphenolic content. However, the molecular mechanism(s) underlying the anti-cancer effects of ABE in CRC remain unclear, which is important to consider when considering their use as complementary medicine approaches in cancer.
methodsWe performed genome-wide transcriptomic profiling and pathway enrichment analysis to identify specific growth signaling pathways associated with ABE treatment in CRC cells. In addition, a series of systematic and comprehensive cell culture studies were performed to investigate the anti-cancer effects of ABE in SW480 and HCT116 CRC cell lines. Subsequently, these findings were validated in patient-derived 3D organoids (PDOs) models.
resultsTranscriptomic profiling analysis identified p53 signaling as one of the key enriched pathways mediating the anti-cancer activity of ABE. Analysis of public datasets revealed that Chk1, a key regulator of p53, was one of the critical targets of ABE in CRC. Chk1 and p53 activation was shown to be downregulated with ABE treatment, leading to the induction of cell cycle arrest (p = 0.003-0.014) and enhanced DNA damage (p = 0.015-0.026). Furthermore, these findings were validated in PDOs, where the ABE treatment resulted in significantly fewer and smaller PDOs in a concentration-dependent manner (p = 0.045 - <0.001).
conclusionsWe firstly provide evidence for the role of the p53 signaling pathway as a mediator of the anti-cancer activity of ABE, which provides a rationale for its use as a safe and effective integrative medicine approach in CRC.
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