Stressing Out Cancer: Chronic Stress Induces Dysbiosis and Enhances Colon Cancer Growth

Author:

McCollum Shannon E.12ORCID,Shah Yatrik M.234ORCID

Affiliation:

1. 1Cellular and Molecular Biology Program, University of Michigan, Ann Arbor, Michigan.

2. 2Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan.

3. 3Department of Internal Medicine, Division of Gastroenterology, University of Michigan, Ann Arbor, Michigan.

4. 4Rogel Cancer Center, University of Michigan, University of Michigan, Ann Arbor, Michigan.

Abstract

Abstract Psychologic stress significantly impacts colorectal cancer, and chronic stress is known to decrease treatment efficacy and survival rates in patients with colorectal cancer. Previous studies have linked psychologic stress to changes in the gut microbiota, and the role of the microbiota in colorectal cancer progression is well characterized. Despite this, the mechanistic link between chronic stress and colorectal cancer remains unclear. In this issue of Cancer Research, Cao and colleagues reveal that chronic stress exacerbates colorectal cancer progression by reducing the presence of Lactobacillus johnsonii (L. johnsonii) and its metabolite protocatechuic acid (PCA). The authors demonstrate an increase in β-catenin expression as the major mechanism by which chronic stress potentiates cancer stemness and pathogenesis. Administration of L. johnsonii or PCA to stressed mice decreased β-catenin activity and colorectal cancer progression. This study defines a precise mechanism underlying chronic stress and colorectal cancer progression, emphasizing the relevance of psychologic well-being in colorectal cancer outcome. In addition, the study demonstrates the potential efficacy of L. johnsonii or PCA supplementation as promising therapeutics for colorectal cancer treatment. See related article by Cao et al., p. 771

Publisher

American Association for Cancer Research (AACR)

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