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Tannin, Tannase and Anticancer Activities · Journal article
Biomedicine & Pharmacotherapy · September 2, 2026
Early or partial results. Treat as a signal, not a conclusion.
This in vitro study demonstrates that omega-3 fatty acids (EPA:DHA) plus EGCG modulate stemness-related signaling pathways in patient-derived colorectal organoids exposed to obesity-mimicking adipokine conditions. The treatment reduced CD44 and HES1 expression and suppressed Wnt target genes, but the work is limited to molecular endpoints in organoids and does not establish clinical efficacy or prevention of obesity-associated colorectal cancer.
In vitro mechanistic study using patient-derived organoids. Patient-derived organoids derived from normal colonic mucosa of non-obese CRC patients; tissue samples from obese and non-obese CRC patients for CD133 and CD44 expression analysis. Intervention: Adipocyte-conditioned medium (obesogenic-like stimuli) with EPA:DHA (1:1) plus EGCG (EDE), and Notch1 inhibition with DAPT. Compared with: Adipocyte-conditioned medium alone (OB-EDE) and control (untreated PDOs from non-obese donors).
Obese CRC tissues showed a shift from CD133-high/CD44-low to CD44-high/CD133-low phenotype compared with non-obese CRC In PDOs, EPA:DHA-EGCG (EDE) reduced CD44 and HES1 expression compared with obesogenic stimuli alone (OB-EDE) EDE further reduced Wnt target gene expression and reduced p-S6R to control levels versus OB-EDE
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
This preclinical mechanistic work suggests omega-3 fatty acids and EGCG may counteract obesity-driven changes in colorectal stem cell signaling. However, the lack of animal models, clinical data, or functional assays of cancer prevention means the findings should not yet inform clinical practice or patient recommendations.
This is an in vitro organoid study without clinical outcomes, animal models, or randomized comparison; it demonstrates mechanistic effects of a nutrient combination on signaling pathways in patient-derived tissue but lacks evidence of efficacy in humans or disease prevention.
As stated by the source record.
Quoted from the source exactly as published.
This preclinical mechanistic work suggests omega-3 fatty acids and EGCG may counteract obesity-driven changes in colorectal stem cell signaling. However, the lack of animal models, clinical data, or functional assays of cancer prevention means the findings should not yet inform clinical practice or patient recommendations.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Obesity is a major risk factor for colorectal cancer (CRC), promoting tumor initiation through chronic inflammation and metabolic dysregulation. Cancer stem cells (CSCs) drive CRC progression through Notch1, Wnt/β-catenin (Wnt), and PI3K/mTOR (mTOR) signaling. Omega-3 polyunsaturated fatty acids (EPA and DHA) and epigallocatechin-3-gallate (EGCG) may modulate these pathways. This study investigated the effects of obesogenic-like stimuli on CSC-related CRC signaling and the preventive potential of EPA:DHA-EGCG in patient-derived organoids (PDOs) from normal mucosa (NM) of non-obese (non-OB) patients. CD133 and CD44 expression was evaluated in tumor tissues and matched NM from obese (OB) and non-OB CRC patients. PDOs derived from NM of non-OB patients were exposed to an adipocyte-conditioned medium reproducing an obesogenic adipokine profile, with or without EPA:DHA (1:1) plus EGCG (EDE). Viability, morphology, and molecular markers of stemness, differentiation, and CRC-related pathways were assessed. OB CRC tissues exhibited a CSC change from CD133-high/CD44-low to CD44-high/CD133-low compared with non-OB CRC. In PDOs, OB-EDE recapitulated this CD44-high/CD133-low phenotype, increasing organoid viability and size while maintaining KRT20 comparable to control (CTRL). HES1 was significantly upregulated, consistent with modulation of Notch1 signaling. OB-EDE downregulated Wnt target genes and increased the mTOR downstream effector p-S6R. OB + EDE exerted marker- and pathway-specific effects, maintaining PROM1 at CTRL levels, reducing CD44 and HES1, and increasing KRT20, while LGR5 remained suppressed. Compared with OB-EDE, OB + EDE further reduced the expression of Wnt target genes and reduced p-S6R to CTRL, whereas p-mTOR/mTOR was not significantly affected. Overall, obesogenic-like stimuli were associated with a CD44-high stem-like phenotype accompanied by coordinated changes in Notch1, Wnt and mTOR signaling. EDE exerted differential effects on these molecular alterations, supporting its potential as a complementary bioactive strategy in obesity-associated CRC. Pharmacological inhibition using DAPT provided preliminary functional support for a contribution of Notch1 signaling to the maintenance of this obesogenic phenotype.
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