HDAC5 Depletion Promotes Hyper-Acetylation of FOXA1 and Potentiating HIF1α Transcriptional Activation in Pancreatic Cancer

ABSTRACT: 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 HIF1? signaling via FOXA1. To further validate our hypothesis, we performed the ChIP-seq of relevant proteins in our working model to determine HDAC5?s impact on FOXA1-HIF1? signaling.

ORGANISM(S): Homo sapiens

PROVIDER: GSE263573 | GEO | 2026/02/28

REPOSITORIES: GEO