Fig. 7: GRAMD1A promoted CRC proliferation through facilitating cholesterol metabolism. | Cell Death & Differentiation

Fig. 7: GRAMD1A promoted CRC proliferation through facilitating cholesterol metabolism.

From: KRAS mutation increases histone H3 lysine 9 lactylation (H3K9la) to promote colorectal cancer progression by facilitating cholesterol transporter GRAMD1A expression

Fig. 7

A Gene ontology (GO) enrichment analysis of up-regulated genes detected by RNA-seq after GRAMD1A overexpression in HCT116 cells. B, C Gene set enrichment analysis (GSEA) of cholesterol metabolism and biosynthesis pathways after GRAMD1A overexpression in HCT116 cells. D Heatmap of mRNA level determined by RNA-seq of enzymes involved in de novo cholesterol biosynthesis in HCT116 cells overexpressing GRAMD1A or vector. E Principal component analysis (PCA) score plot and F volcano plot of metabolites determined by metabolomics in HCT116 cells overexpressing GRAMD1A or vector. G Combined KEGG analysis of RNA-seq and metabolomics of HCT116 cells overexpressing GRAMD1A or vector. H Filipin staining of cholesterol levels and immunofluorescence staining of GRAMD1A expression in HCT116 and DLD1 cells overexpressing GRAMD1A or vector. Scale bar: 50 μm. Statistical immunofluorescence results of cholesterol levels and GRAMD1A expression in I HCT116 and J DLD1 cells. n  =  5. Tumor growth of HCT116 and DLD1 cells after GRAMD1A overexpression and 5 μM Simvastatin treatment evaluated by K colony formation assay and L statistical analysis. n  =  3. Tumor growth of HCT116 and DLD1 cells after GRAMD1A overexpression and 5 μM Simvastatin treatment evaluated by M sphere formation assay and N statistical analysis. Scale bar: 500 μm. n  =  3. Values are presented as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, determined by two-tailed Student’s t-test (I, J) and one-way ANOVA (L, N).

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