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Mechanisms of Cancer Metastasis / Cancer, Stress, Anesthesia, and Immune Response / Cancer Research and Treatments · Journal article
Scientific Reports · September 7, 2026
Early or partial results. Treat as a signal, not a conclusion.
This is an in vitro mechanistic study showing that quercetin-exposed Lactobacillus rhamnosus produces a cell-free supernatant with enhanced anti-cancer activity against SW-480 colorectal adenocarcinoma cells and anti-angiogenic effects in a chick chorioallantoic membrane model. The findings are exploratory and demonstrate metabolic reprogramming but do not establish efficacy in animals or humans.
In vitro mechanistic study using cell-free supernatant from quercetin-exposed Lactobacillus rhamnosus against colorectal cancer cells and angiogenesis model. Laboratory-cultured SW-480 colorectal adenocarcinoma cells; pathogenic reference bacteria; chick embryos for angiogenesis model.. Intervention: Cell-free supernatant from Lactobacillus rhamnosus PTCC 1637 pre-exposed to quercetin (up to 200 µg/mL). Compared with: Cell-free supernatant from untreated Lactobacillus rhamnosus PTCC 1637.
Que-CFS lowered 48-h IC₅₀ to 28.36% (v/v) versus 65.7% for untreated CFS in SW-480 cells Flow cytometry revealed 87.4% apoptosis with que-CFS and 57.9% reduction in nuclear area by DAPI staining Que-CFS suppressed wound closure by 26.5% at 48 h and reduced 3-D spheroid volume by 27% at 96 h
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This exploratory work identifies a potential probiotic-metabolite approach to colorectal cancer inhibition through dietary quercetin enhancement, but clinicians should not consider this evidence for patient application pending animal efficacy studies and human trials.
In vitro mechanistic study demonstrating enhanced probiotic metabolite activity against colorectal cancer cells and angiogenesis, but lacking in vivo efficacy data, clinical endpoints, or human translation.
As stated by the source record.
Quoted from the source exactly as published.
This exploratory work identifies a potential probiotic-metabolite approach to colorectal cancer inhibition through dietary quercetin enhancement, but clinicians should not consider this evidence for patient application pending animal efficacy studies and human trials.
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Abstract Colorectal cancer (CRC) is the second leading cause of cancer death worldwide, with rising incidence projected over the coming decades. Here we show that prolonged exposure of Lactobacillus rhamnosus PTCC 1637 to quercetin (up to 200 µg/mL) improves its probiotic traits and markedly boosts the anticancer activity of its cell-free supernatant (que-CFS). Acid tolerance increased, and antibacterial zones against Staphylococcus aureus, Salmonella typhi, and Escherichia coli grew by 2–13 % using que-CFS compared with untreated CFS. In SW-480 colorectal adenocarcinoma cells, que-CFS lowered the 48-h IC₅₀ to 28.36 % (v/v) versus 65.7 % for CFS. Flow cytometry revealed 87.4 % apoptosis with que-CFS; DAPI staining confirmed greater nuclear fragmentation and a 57.9 % reduction in nuclear area. Que-CFS suppressed wound closure by 26.5 % at 48 h, reduced 3-D spheroid volume by 27 % at 96 h, and inhibited angiogenesis in the chick chorioallantoic membrane by 36.3 % versus 23.1 % for CFS. qRT-PCR showed stronger upregulation of Caspase-8, BAX and TP53. Proteinase K abolished antibacterial activity, confirming proteinaceous mediators. These data reveal that quercetin reprograms L. rhamnosus metabolism to yield metabolites with superior cytotoxic, anti-migratory, anti-spheroid, and anti-angiogenic effects, opening a dietary route to potentiate probiotic anticancer therapy.
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