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

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 HIF1α 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE285080 | GEO | 2026/02/28

REPOSITORIES: GEO

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

Project description: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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Histone modifications regulated by HDAC5 in PDAC cells

Project description:HDAC5 belongs to Class IIa histone deacetylases and forms corepressor complex with HDAC3. To understand the epignetic regulations by HDAC5, we performed ChIP-seq analysis of H3K4me3, H3K27ac and H3K9ac in PDAC cells overexpressing GFP or HDAC5, and in HDAC5 escaper cells with HDAC5 knockdown or scramble control.

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HDAC5 loss in pancreatic cancer induces enhanced arachidonic acid metabolism via overactivated GATA1-cPLA2 axis

Project description: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. Additionally, HDAC5’s expression correlates negatively with arachidonic acid (AA) metabolism, which is highly implicated in inflammatory responses and cancer progression. This study aimed to elucidate the role of HDAC5 in AA metabolism and its prospect in the treatment of pancreatic cancer.

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HDAC5-ChIP seq data in HDAC5-driven KRASG12D-independent PDAC cells

Project description:HDAC5 belongs to Class IIa histone deacetylases and forms corepressor complex with HDAC3 to suppess gene expression. To identify the target genes of HDAC5, we performed ChIP-seq analysis in FLAG-tagged HDAC5 PDAC escaper cells. HDAC5 binding chromatins were pulled down by HDAC5 antibody and FLAG antibody as replicates.

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HDAC5 is a repressor of angiogenesis and determines the angiogenic gene expression pattern of endothelial cells

Project description:Class IIa histone deacetylases (HDACs) are signal-responsive regulators of gene expression involved in vascular homeostasis. To investigate the differential role of class IIa HDACs for the regulation of angiogenesis, we used siRNA to specifically suppress the individual HDAC isoenzymes. Among the HDAC isoforms tested, silencing of HDAC5 exhibited a unique pro-angiogenic effect evidenced by increased endothelial cell migration, sprouting and tube formation. Consistently, overexpression of HDAC5 decreased sprout formation, indicating that HDAC5 is a negative regulator of angiogenesis. The anti-angiogenic activity of HDAC5 was independent of MEF2 binding and its deacetylase activity, but required a nuclear localization indicating that HDAC5 might affect the transcriptional regulation of gene expression. To identify putative HDAC5 targets, we performed microarray expression analysis. Silencing of HDAC5 increased the expression of fibroblast growth factor 2 (FGF2) and angiogenic guidance factors including Slit2. Antagonization of FGF2 or Slit2 reduced sprout induction in response to HDAC5 siRNA. ChIP assays demonstrate that HDAC5 binds to the promoter of FGF2 and Slit2. In summary, HDAC5 represses angiogenic genes, like FGF2 and Slit2, which causally contribute to capillary-like sprouting of endothelial cells. The de-repression of angiogenic genes by HDAC5 inactivation may provide a useful therapeutic target for induction of angiogenesis.

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RNAi of human HUVEC cells knocked down for HDAC isoenzymes reveals sHDAC5 is a repressor of angiogenesis and determines the angiogenic gene expression pattern of endothelial cells

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HDAC5, an early osimertinib-responsive gene, is a novel therapeutic target for the drug resistance in EGFR-mutant lung adenocarcinoma cells.

Project description:Aberrant epigenetic regulation is closely associated with drug tolerance, an early step in the acquisition of drug resistance. We previously reported that a pioneer transcriptional factor (also called an epigenetic initiator) rapidly induced by osimertinib, a third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, plays a pivotal role in promoting the formation of osimertinib-tolerant cells. In this study, to identify novel epigenetic factors associated with osimertinib-tolerance, we performed a comprehensive screening of epigenetic factors whose expression is rapidly induced by osimertinib. Our results revealed that HDAC5, a class IIa histone deacetylase (HDAC), is the most prominently induced epigenetic factor in EGFR-mutant non-small cell lung cancer (NSCLC) cell lines during the early response to osimertinib. Knockdown of HDAC5 significantly reduced the emergence of osimertinib-resistant cells. Furthermore, treatment with LMK235, a selective HDAC5 inhibitor, significantly increased global histone acetylation and enhanced osimertinib-induced apoptosis. These findings underscore the potential of HDAC5 as a novel therapeutic target to overcome osimertinib-resistance and propose LMK235 as a promising compound to provide significant therapeutic benefits for EGFR-mutant NSCLC patients undergoing osimertinib treatment.

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

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

| PRJNA1098083 | ENA

Transcriptome profiling of human urothelial carcinoma cell lines RT-112, VM-Cub-1, SW1710, UMUC3 and a benign urothelial control HBLAK engineered to stably express HDAC5 against their vector control

Project description:Aberrant expression of histone deacetylases (HDACs) and their activity are associated with a broad range of tumor development. However, based on cell or tissue types, class IIA HDACs such as HDAC4 and HDAC5 may facilitate or inhibit cancer progression. The goal of this project is to examine the gene expression changes caused by HDAC5 expression. Here, we studied the effects of stable expression of HDAC5 (that is normally downregulated or have a weak basal expression) in four urothelial carcinoma (UC) cell lines (RT112, VM-Cub-1, SW1710, and UM-UC-3) by rRNA-depleted RNA-sequencing in comparison to their vector controls. We observed that HDAC5 expression in VM-Cub-1 triggered a drastic phenotype change from an epitheloid to a mesenchymal (i.e., epithelial-mesenchymal transition, EMT) and altogether diminished cell proliferation of the other three cell lines. Our RNA-seq data are in line with the phenotypic transformation of VM-Cub-1. In addition, we also performed a gene expression profiling of HBLAK, a spontaneously immortalized from primary human bladder epithelial cells that can be directly compared with the four UC vector cells. HBLAK vector cells only were included for RNA-seq as the cells failed to express HDAC5 after lentiviral transduction and selection.

2019-11-13 | E-MTAB-8418 | biostudies-arrayexpress

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

Project description:HDAC5 Depletion Promotes Hyper-Acetylation of FOXA1 and Potentiating HIF1α Transcriptional Activation in Pancreatic Cancer [ATAC-Seq]

| PRJNA1201154 | ENA

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