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Analyzing the Epigenomic Effects of Butyrate on Human Colon Cancer Cells

Cribas, Emily S.1; Fremin, Brayon J.2; and Bhatt, Ami S.2
1
Pennsylvania State University, University Park, Pennsylvania
2
Department of Genetics, Stanford University School of Medicine, Stanford, California
Commensal bacteria within the human colon produce a metabolite known as butyrate
through fiber fermentation. Studies show butyrate induces expression of a differentiation
marker in a subset of human colon cancer cells. This suggests that butyrate induces
differentiation of cells, which has been explored as a method of cancer therapy. It is
hypothesized that butyrate induces differentiation through its role in histone deacetylase
(HDAC) inhibition. HDAC inhibition induces decondensation of chromatin and an
increase in chromatin accessibility. The whole-epigenomic effects of butyrate on different
subsets of colon cancer cells remain unknown. We hypothesize that butyrate results in
differential chromatin decondensation in various colon cancer cell lines. Furthermore, we
hypothesize that the extent and pattern of decondensation will be different between those
cell lines that differentiate in response to butyrate treatment vs. those that do not. In this
study, we perform ATAC-Seq, an assay for tranposase-accessible (open) chromatin on
different subsets, to assess areas where the chromatin has been decondensed in response
to butyrate. The results from these experiments provide a genome-wide perspective on
what genes are exclusively affected by butyrate HDAC inhibition. Further studies linking
these affected genes with induced differentiation are needed to elucidate the role of
butyrate, or a high-fiber diet, in serving as a cancer differentiation therapy.