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HDAC5 expression was positively correlated with miR-2861 in lung cancer stem cells (LCSCs), and knockdown of miR-2861 decreased the expression of HDAC5, which implied that HDAC5 may be involved in the differentiation of LCSCs mediated by miR-2861.
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These results demonstrate a previously unknown negative epigenetic regulation of hematopoietic stem cells (HSC) homing and engraftment by HDAC5, and allow for a new and simple translational strategy to enhance HSC transplantation.
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Collectively, these data indicate that vIRF3 alters global gene expression and induces a hypersprouting formation in an HDAC5-binding-dependent and lymphatic endothelial cell-specific manner, ultimately contributing to Kaposi's sarcoma-associated herpesvirus-associated pathogenesis.
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High HDAC5 expression is associated with invasion of lung cancer.
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HO-1 plays a key role in protecting tumor cells from apoptosis, in a process that involves Smad7 and HDAC4/5 in apoptosis of B-ALL cells
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Hdac5 and Hdac6 expression are required for the adequate expression of Icer and adipocyte function. Altered adipose expression of the two Hdacs in obesity by hypoxia may contribute to the development of metabolic abnormalities.
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These findings demonstrate a novel mechanism for deregulation of HDAC5 in non-small cell lung cancer (NSCLC)and suggest that miR5895p/HDAC5 pathway may represent a new prognostic biomarker and therapeutic target against NSCLC.
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HDAC5 was extensively expressed in human BC tissues, and high HDAC5 expression was associated with an inferior prognosis.
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HDAC5 is a negative predictor of disease-free and overall survival in pancreatic neuroendocrine tumor patients.
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Interference with both glucose and glutamine supply in HDAC5-inhibited cancer cells significantly increases apoptotic cell death.
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these results suggest that HDAC5 is critical in regulating LSD1 protein stability through post-translational modification, and the HDAC5-LSD1 axis has an important role in promoting breast cancer development and progression.
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The expression of HDAC5 was significantly increased in endothelial cells (ECs) from patients with systemic sclerosis (SSc) compared to healthy control endothelial cells. Silencing of HDAC5 in SSc ECs restored normal angiogenesis. HDAC5 knockdown followed by ATAC-seq assay in SSc ECs identified key HDAC5-regulated genes involved in angiogenesis and fibrosis, such as CYR61, PVRL2, and FSTL1.
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the migration and invasion of hepatocellular carcinoma cells were impaired by knockdown of histone deacetylase 5 or hypoxia-inducible factor-1alpha but rescued when eliminating homeodomain-interacting protein kinase-2 in hepatocellular carcinoma cells, which suggested the critical role of histone deacetylase 5-homeodomain-interacting protein kinase-2-hypoxia-inducible factor-1alpha pathway in hypoxia-induced metastasis.
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HDAC5 inhibits hepatic lipogenic genes expression by attenuating the transcriptional activity of liver X receptor.
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HDAC5 promotes cellular proliferation through the upregulation of cMet, and may provide a novel therapeutic target for the treatment of patients with Wilms' tumor.
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HDAC5 and HDAC6 were highly expressed in melanoma cells but exhibited low expression levels in normal skin cells.
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Formononetin-combined therapy may enhance the therapeutic efficacy of doxorubicin in glioma cells by preventing EMT through inhibition of HDAC5.
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These results suggest a strong regulatory function of HDAC5 in the pro-inflammatory response of macrophages.
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In erythroid cells, pull down experiments identified the presence of a novel complex formed by HDAC5, GATA1, EKLF and pERK which was instead undetectable in cells of the megakaryocytic lineage.
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Data reveal a novel role of HDAC5 in modulating the KLF2 transcriptional activation and eNOS expression.
