Investigation shows how bacterial adhesins contribute to colon cancer mutations, suggesting new avenues for therapeutic intervention in colorectal cancer.
By Dr. Chinta SidharthanReviewed by Danielle Ellis, B.Sc.Nov 7 2024 Research uncovers how bacterial surface adhesion proteins initiate mutations in colon cells, highlighting potential targets for cancer prevention strategies.
Background Colorectal cancer affects more than two million individuals worldwide every year and is one of the leading causes of cancer-associated mortality. Studies show that the disease is linked to Western lifestyles consisting of inadequate physical activity and unhealthy diets, and the incidence of colorectal cancer is rising, especially among people below 50 years of age.
Studies from human intestinal organoids have reported that colibactin directly binds to the DNA, causing mutations that are often detected in colorectal cancer patients. However, the processes that allow the pks+ E. coli direct contact with the intestinal cells and the mechanisms through which colibactin reaches the host cell DNA remain unclear.
Related StoriesThe inflammation levels were determined by analyzing the inflammatory markers such as C-X-C motif chemokine ligand 1 and interleukins 17A and 1β. Additionally, transcriptomic analysis was performed to examine the expression of tumor-related genes in the epithelial and immune cells of the colon.
Furthermore, in comparison to the control strain of E. coli, which remained in the gut lumen, the pks+ E. coli 11G5 strain was able to strongly adhere to the epithelial cells and invade the gut lining, forming large bacterial colonies that were directly associated with the epithelial cells of the colon. This suggested that the pks+ E. coli 11G5 strain promoted colorectal cancer progression by infiltrating the colonic tissue.
Cancer Colon Colon Cancer Cancer Prevention Cell Colorectal Colorectal Cancer DNA DNA Damage Dysbiosis Genes Inflammation Microbiome Mortality Physical Activity Research Toxin Tumor
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