ArticleInternational journal of molecular sciences2019
HDAC5 Expression in Urothelial Carcinoma Cell Lines Inhibits Long-Term Proliferation but Can Promote Epithelial-to-Mesenchymal Transition.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Association of changes in expression ofEpigenetics · 2024Article
- Targeting histone modifiers in bladder cancer therapy - preclinical and clinical evidence.Nature reviews. Urology · 2024Review
- N6-methyladenosine methylation in kidney injury.Clinical epigenetics · 2023Review
- Synergistic Interaction of the Class IIa HDAC Inhibitor CHDI0039 with Bortezomib in Head and Neck Cancer Cells.International journal of molecular sciences · 2023Article
- Epigenetic Priming and Development of New Combination Therapy Approaches.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Proteomic and transcriptomic profiles of human urothelial cancer cells with histone deacetylase 5 overexpression.Scientific data · 2022Article
- Pan-cancer quantitation of epithelial-mesenchymal transition dynamics using parallel reaction monitoring-based targeted proteomics approach.Journal of translational medicine · 2022Article
- Alterations of Chromatin Regulators in the Pathogenesis of Urinary Bladder Urothelial Carcinoma.Cancers · 2021Review
- Article
- METTL14-regulated PI3K/Akt signaling pathway via PTEN affects HDAC5-mediated epithelial-mesenchymal transition of renal tubular cells in diabetic kidney disease.Cell death & disease · 2021Article
- Insights Into the Function and Clinical Application of HDAC5 in Cancer Management.Frontiers in oncology · 2021Review
- Unresolved Complexity in the Gene Regulatory Network Underlying EMT.Frontiers in oncology · 2020Review
- Epigenetics of Urological Cancers.International journal of molecular sciences · 2019Article
- Proteomic Technology "Lens" for Epithelial-Mesenchymal Transition Process Identification in Oncology.Analytical cellular pathology (Amsterdam) · 2019Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Class I histone deacetylases (HDACs) generally promote cell proliferation and tumorigenesis, whereas class IIA HDACs like HDAC4 and HDAC5 may promote or impede cancer development in a tissue-dependent manner. In urothelial carcinoma (UC), HDAC5 is often downregulated. Accordingly, HDAC5 was weakly expressed in UC cell lines suggesting a possible tumor-suppressive function. We therefore characterized the effects of stable HDAC5 expression in four UC cell lines (RT112, VM-Cub-1, SW1710 and UM-UC-3) with different phenotypes reflecting the heterogeneity of UC, by assessing proliferation, clonogenicity and migration ability. Further, we detailed changes in the proteome and transcriptome by immunoblotting, mass spectrometry and RNA sequencing analysis. We observed that HDAC5 overexpression in general decreased cell proliferation, but in one cell line (VM-Cub-1) induced a dramatic change from an epitheloid to a mesenchymal phenotype, i.e., epithelial-mesenchymal transition (EMT). These phenotypical changes were confirmed by comprehensive proteomics and transcriptomics analyses. In contrast to HDAC5, overexpression of HDAC4 exerted only weak effects on cell proliferation and phenotypes. We conclude that overexpression of HDAC5 may generally decrease proliferation in UC, but, intriguingly, may induce EMT on its own in certain circumstances.
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