Barley polysaccharides inhibit colorectal cancer by two relatively independent pathways

Cheng Zhang1, Li Li1, Jiali Lin1

  • 1Department of Food Science and Engineering, Jinan University, Guangzhou 510630, China.

Insights

Barley polysaccharides (BP) show significant potential in inhibiting colorectal cancer. BP acts directly by promoting protective metabolites and indirectly by enriching beneficial gut bacteria, offering a dual-action approach to cancer prevention.

Area of Science:

  • Gastroenterology
  • Oncology
  • Microbiome research

Background:

  • Colorectal cancer is a leading global health concern.
  • Polysaccharides are known for antitumor properties, but barley polysaccharides (BP) role is understudied.
  • Understanding BP's impact on colorectal cancer is crucial.

Purpose of the Study:

  • To investigate the anti-colorectal cancer effects of barley polysaccharides (BP).
  • To elucidate the mechanisms underlying BP's inhibitory action on colorectal cancer.
  • To explore the dual role of BP in direct and gut microbiota-mediated pathways.

Main Methods:

  • In vivo administration of BP (300 mg/kg) to assess colorectal cancer inhibition.
  • Analysis of metabolite production and cancer pathway modulation.
  • Gut microbiota profiling and assessment of intestinal barrier function.

Main Results:

  • BP (300 mg/kg) significantly inhibited colorectal cancer progression.
  • BP promoted protective metabolites (e.g., 5-(4-Hydroxyphenyl)-5-phenylimidazolidine-2,4-dione) and inhibited cancer pathways (ERK, PI3K, WNT, JAK-STAT, Cell cycle).
  • BP enriched beneficial bacteria (Colidextribacter, Bilophila, UCG-003), improved gut barrier, and modulated metabolites (L-Glutamic acid) and pathways (Apoptosis, TGF-β).

Conclusions:

  • Barley polysaccharides (BP) demonstrate significant colorectal cancer inhibitory effects.
  • BP acts through direct promotion of protective metabolites and indirect modulation of the gut microbiota.
  • These findings highlight BP as a potential therapeutic agent for colorectal cancer via a dual-action mechanism.

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