Fig. 5: Gene signatures of cholesterol biosynthesis are enriched in transcriptomic datasets of human colorectal neoplasia. | Communications Biology

Fig. 5: Gene signatures of cholesterol biosynthesis are enriched in transcriptomic datasets of human colorectal neoplasia.

From: BRAFV600E-mutated serrated colorectal neoplasia drives transcriptional activation of cholesterol metabolism

Fig. 5: Gene signatures of cholesterol biosynthesis are enriched in transcriptomic datasets of human colorectal neoplasia.

a, b GSEA showing increased expression of the cholesterol gene signature in human serrated lesions (SSL) from three independent datasets comparing serrated neoplasia to normal matched control (a) or to adenomatous lesions (AD). NES normalized enrichment score. (b). c UMAP visualization of cells from serrated and normal datasets colored by annotated cell type. ABS absorptive cells, CT crypt top colonocytes, EE enteroendocrine cells, GOB goblet cells, SSC serrated specific cells, STM stem cells, TAC transient amplifying cells, TUF tuft cells. d UCell score distribution for the cholesterol gene signature shown in UMAP space. e Violin plot showing a comparison of UCell score distribution of a cholesterol gene signature in different cell populations. The boxes represent median and interquartile ranges. The whiskers show 95% confidence interval. The distribution of UCell score in SSC population was compared with the remaining cell lineages using the Wilcoxon statistical test. ****P ≤ 0.0001.

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