GEO series
HDAC5 Depletion Promotes Hyper-Acetylation of FOXA1 and Potentiating HIF1α Transcriptional Activation in Pancreatic Cancer
GSE263573
Homo sapiens
Genome binding/occupancy profiling by high throughput sequencing
32 samples
2026/02/28
GPL11154
Summary
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.
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