Skip to main content
NUTRITION 2024 Main banner
Icon Legend
This session is not in your schedule.
This session is in your schedule. Click again to remove it.
Back

Session: Dietary Patterns and Components in Cancer Risk and Survivorship (Poster Theater Flash Session 6)

(PTFS06-06-24) The Protective Potential of Butyrate Against Colon Cancer Cells Is Critically Dependent on Cell Type

Sunday, June 30, 2024
12:20 PM – 12:24 PM CT
Location:  W185A-C

    Presenting Author(s)

  • SO

    Sema Oncel, PhD (she/her/hers)

    Postdoctoral Fellow
    USDA-ARS Grand Forks Human Nutrition Research Center
    Grand Forks, North Dakota, United States

    Disclosure(s): No relevant financial relationship(s) with ineligible companies to disclose.

    • Co-Author(s)

  • JL

    James Lindlauf

    USDA/ARS, United States

  • HZ

    Huawei Zeng, PhD

    Research Molecular Biologist
    USDA-ARS Grand Forks Human Nutrition Research Center
    Grand forks, North Dakota, United States

Objectives: Short-chain fatty acids such as butyrate are produced through the fermentation of dietary fiber by colonic bacteria. Preclinical studies indicate that butyrate exhibits anti-cancer properties; however, clinical evidence shows greater variability. We hypothesized that butyrate displays greater effectiveness in influencing cell proliferation, cell migration, and invasion in highly aggressive HCT116 human colon cancer cells compared to less aggressive HT29 and Caco-2 cells.

Methods: We, first, determined half maximal inhibitory concentrations (IC50) of butyrate (0 to 4 mM) in HCT116, HT-29, and Caco-2 cell growth at 24, 48, and 72 h. Then, we used wound closure assay, invasion assay, and western blotting to determine anti-motogenic efficacy of butyrate on these three differentially divergent colon cancer cells.

Results: The IC50 (mM) butyrate concentrations of HCT116, HT-29, and Caco-2 cells were [24 h, 1.14; 48 h, 0.83; 72 h, 0.86], [24 h, N/D; 48 h, 2.42; 72 h, 2.15], and [24 h, N/D; 48 h, N/D; 72 h, 2.15], respectively. Butyrate decreased wound closure ( > 20%) in HCT116 cells (but not in HT-29 and Caco-2 cells) when treated with 2 mM butyrate. Likewise, % decrease in invasion after butyrate treatment (mM) were greatest in HCT116 cells ( > 60%, 0.5 mM) followed by HT-29 ( > 60%, 2 mM) and Caco-2 cells ( > 60%, 4 mM). Correspondingly, activation of key proteins for migration and invasion were decreased at 1 mM ( > 40%, FAK) and at 0.25 mM ( > 20%, Src) in HCT116 cells but not changed in HT-29 and Caco-2 cells. Conversely, cellular E-cadherin, a classical epithelial cell marker, increased ( > 60%) in HCT116 cells and ( > 10%) in HT-29 cells at 2 mM while not changing in Caco-2 cells.

Conclusions: Collectively, butyrate’s anti-cancer efficacy on colon cancer cells in vitro varies depending on cell-type and linked to the FAK/Src/E-Cadherin pathway.

Funding Sources: This work was supported by U.S. Department of Agriculture, Agricultural Research Service, research project 3062-51000-056-00D.