Journal of agricultural and food chemistryAug 26, 2024

Lactobacillus plantarum may improve colorectal cancer by strengthening the gut barrier through the CLA-PPAR-γ pathway

Circadian Biology Weekly Brief ↗PubMed ↗DOI ↗

Updated Mar 28, 2026

Abstract

CCFM8661 treatment significantly ameliorated colorectal cancer (CRC) in Apc mice compared to phosphate-buffered solution treatment.

Conjugated linoleic acid (CLA) was identified as a key metabolite responsible for the effects of CCFM8661 on CRC.
The peroxisome proliferator-activated receptor γ (PPAR-γ) was shown to be a crucial receptor in the amelioration of CRC.
CCFM8661 may inhibit the NF-κB pathway and pro-inflammatory cytokines while promoting the expression of ZO-1, Claudin-1, and MUC2.
The treatment appears to enhance tumor cell apoptosis in a manner dependent on PPAR-γ.
Metagenomic analysis indicated that CCFM8661 treatment may repair the intestinal barrier, which is associated with CRC improvement.
Clinical results showed decreased levels of intestinal CLA, butyric acid, and PPAR-γ in CRC patients, correlating negatively with the disease.

Simplified

Colorectal cancer (CRC) is the third-largest cancer worldwide.can regulate the intestinal barrier and gut microbiota. However, the mechanisms ofthat alleviate CRC remained unknown. This study aimed to explore the regulatory effect ofon CRC and its potential mechanism. CCFM8661 treatment significantly ameliorated CRC compared with phosphate-buffered solution (PBS) treatment in Apcmice. In addition, conjugated linoleic acid (CLA) was proved to be the key metabolite for CCFM8661 in ameliorating CRC by molecular biology techniques. Peroxisome proliferator-activated receptor γ (PPAR-γ) was proved to be the key receptor in ameliorating CRC by inhibitor intervention experiments. Moreover, supplementation with CCFM8661 ameliorated CRC by producing CLA to inhibit NF-κB pathway and pro-inflammatory cytokines, up-regulate ZO-1, Claudin-1, and MUC2, and promote tumor cell apoptosis in a PPAR-γ-dependent manner. Metagenomic analysis showed that CCFM8661 treatment significantly increased, which could ameliorate CRC by repairing the intestinal barrier. Clinical results showed that intestinal CLA, butyric acid, PPAR-γ, andwere significantly decreased in CRC patients, and these indicators were significantly negatively correlated with CRC. CCFM8661 alleviated CRC by ameliorating the intestinal barrier through the CLA-PPAR-γ axis. These results will promote the development of dietary probiotic supplements for CRC. Lactobacillus Lactobacillus Lactobacillus plantarum Odoribacter splanchnicus Lactobacillus Min/+

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Lactobacillus plantarum may improve colorectal cancer by strengthening the gut barrier through the CLA-PPAR-γ pathway

Abstract

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