Fig. 7: DHX9 represses BECN1 transcription via histone deacetylation. | Cell Death & Disease

Fig. 7: DHX9 represses BECN1 transcription via histone deacetylation.

From: DHX9-mediated epigenetic silencing of BECN1 contributes to impaired autophagy and tumor progression in breast cancer via recruitment of HDAC5

Fig. 7: DHX9 represses BECN1 transcription via histone deacetylation.

A Gene Ontology-Biological Process analysis indicated that gene sets related to histone modification were enriched in the DHX9 high expression group. B, C Immunoblot analysis revealed the impact of DHX9 silencing (B) or augmentation (C) on the acetylation level of histone H3. D, E Immunoblot analysis revealed the effect of HDAC5 silencing (D) or augmentation (E) on the acetylation level of histone H3. F, G Immunoblot analysis revealed that DHX9-mediated deacetylation of histone H3 depended on HDAC activity (F) or HDAC5 (G). H, I ChIP-qPCR showed the enrichment levels of Ace-H3 or HDAC5 on BECN1 promoter after DHX9 downregulation. J A sketch map to elucidate the biological function of DHX9 in BC. Enhanced expression of DHX9 represses BECN1 transcription by recruiting HDAC5 to its promoter mediating the deacetylation of histone H3 and contributes to impaired autophagy and tumor development in BC. Data are representative of three biological independent experiments (B–I) and are plotted as the mean ± SD (H, I). P values were calculated by unpaired two-tailed Student’s t test (H, I). **p < 0.01 vs. corresponding control.

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