Epidemiological studies have linked increased incidence of inflammatory diseases and intestinal cancers in the developed parts of the world to the consumption of diets poor in dietary fibres and rich in refined carbohydrates. Gut bacteria residing in the intestinal lumen exclusively metabolise dietary fibres and produce butyrate, propionate and acetate, which are collectively called short-chain fatty acids (SCFAs). Evidence is accumulating that SCFA play an important role in the maintenance of gut and metabolic health (1,2,3). Glycans on cells lining the gut have been shown to undergo changes in structure with the onset of diseases such as inflammation and cancer (4). Specifically, mucin glycans are seen as important drivers of the composition and functionality of the gut microbiota (5). Overall, nutrition has been shown to have an impact on the diversity of the gut microbiome and it’s symbiosis with colonic mucosa. It appears that SCFAs increase the expression of epithelial barrier-forming mucins and influence the production of immune cells in the colon (6). Altered glycosylation patterns also are a hallmark of the tumour phenotype with one of the most common changes being an increase in the size and branching of N-linked glycans (7).
In this study we analysed the effect of SCFA treatment on cell differentiation, glycosylation and migration of three different colon cancer cell lines; LIM 1215, LIM1899 and LIM2405. We show that SCFAs have a significant cytotoxicity effect when compared to non-treated colon cancer cells. Cell migration also decreased in all three LIM cell lines after SFCA treatment. These effects of SCFAs on colon cancer cell survival and migration correlated with changes in N- and O-linked protein glycosylation.