Fig. 8: FIBCD1 promotes the enrichment of H3K27ac in the MCM5 promoter region through the PDH-acetyl-CoA axis. | Cell Death & Disease

Fig. 8: FIBCD1 promotes the enrichment of H3K27ac in the MCM5 promoter region through the PDH-acetyl-CoA axis.

From: Diabetes is causally associated with increased breast cancer mortality by inducing FIBCD1 to activate MCM5-mediated cell cycle arrest via modulating H3K27ac

Fig. 8

A UCSC genome browser views for the MCM5 gene, indicating that H3K27ac mark is enriched in the promoter of MCM5. B Upregulation of FIBCD1 increases H3K27Ac level in both MDA-MB-231 and MCF7 cells. C Histone acetylase inhibitor C646 inhibits the effect of FIBCD1 on H3K27ac in BC cells. D Schematic illustration of four potential binding sites (Ch-IP1, Ch-IP2, Ch-IP3, Ch-IP4) in the MCM5 promoter for H3K27ac (top). Agarose gel electrophoresis of PCR products indicates that FIBCD1 increases the binding of H3K27ac with MCM5 promoter (bottom). E ChIP assay shows that H3K27Ac is enriched in the promoter region of MCM5 in MDA-MB-231 cells. F Upregulation of FIBCD1 promotes PDH production from MDA-MB-231 cells. G Overexpression of FIBCD1 augments PDH production from MCF7 cells. H Upregulation of FIBCD1 facilitates acetyl-CoA generation and C646 inhibits acetyl-CoA production from MDA-MB-231 cells. I Overexpression of FIBCD1 increases the release of acetyl CoA but C646 suppresses acetyl CoA production from MCF7 cells. Data are presented as mean ± SD, Student’s t test. *P < 0.05; **P < 0.01; ***P < 0.001.

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