HDAC5 Depletion Promotes Hyper-Acetylation of FOXA1 and Potentiating HIF1a Transcriptional Activation in Pancreatic Cancer [ATAC-Seq]

Unlike class I Histone deacetylase (HDAC) members (HDAC1, 2, 3, etc.), HDAC5, a class IIa HDAC member, is downregulated in multiple solid tumors, including pancreatic cancer, and its loss is associated with unfavorable prognosis. We observed that HDAC5 mediates FOXA1-K270 deacetylation and represses HIF1a signaling via FOXA1. To further validate our hypothesis, we performed the ATAC-seq in control and HDAC5 knockdown PANC-1 cells to test whether HDAC5 knockdown affects chromatin accessibility. Overall design: ATAC-seq were applied in control and HDAC5 knock-down (kd) PANC-1 cells.