ArticleJournal of translational medicine2016
Both HDAC5 and HDAC6 are required for the proliferation and metastasis of melanoma cells.
Article in Journal of translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 69 citations in OpenAlex.
- Enhanced IFNy response in dedifferentiated melanoma cells is due to chromatin remodeling as revealed by ATAC-seq.Cell communication and signaling : CCS · 2026Article
- Epigenetic Modulators and Immunotherapy in Malignant Melanoma.Oncology research · 2026Review
- WT161, a selective HDAC6 inhibitor, decreases growth, enhances chemosensitivity, promotes apoptosis, and suppresses motility of melanoma cells.Cancer chemotherapy and pharmacology · 2025Article
- Histones deacetylases in the epidermis: structure, functions and therapeutic implications.Frontiers in epigenetics and epigenomics · 2025Review
- Targeting lipogenesis promotes the synergistic effect of the selective HDAC6 inhibitor ITF3756 with bortezomib in colon cancer cells.Frontiers in pharmacology · 2025Article
- Association of changes in expression ofEpigenetics · 2024Article
- Temporal regulation of acetylation status determines PARP1 role in DNA damage response and metabolic homeostasis.Science advances · 2024Article
- Identification of SLC22A17 DNA methylation hotspot as a potential biomarker in cutaneous melanoma.Journal of translational medicine · 2024Article
- Circulating tumor cells: from new biological insights to clinical practice.Signal transduction and targeted therapy · 2024Review
- Epigenetic regulation in cancer.MedComm · 2024Review
- Targeting histone deacetylase suppresses tumor growth through eliciting METTL14-modified mCancer communications (London, England) · 2023Article
- The Selective Cytotoxicity of Quercus Brantii Lindl. Galls on A375 and SK-MEL-3 Human Malignant Melanoma Cell Lines.Asian Pacific journal of cancer prevention : APJCP · 2023Article
- Targeting HDAC6 to Overcome Autophagy-Promoted Anti-Cancer Drug Resistance.International journal of molecular sciences · 2022Review
- Epigenetic modification regulates tumor progression and metastasis through EMT (Review).International journal of oncology · 2022Review
- Histone deacetylation regulates nucleotide excision repair through an interaction with the XPC protein.iScience · 2022Article
- Epigenetics Regulates Antitumor Immunity in Melanoma.Frontiers in immunology · 2022Review
- Neratinib kills B-RAF V600E melanoma via ROS-dependent autophagosome formation and death receptor signaling.Pigment cell & melanoma research · 2022Article
- Crosstalk of four kinds of cell deaths defines subtypes of cutaneous melanoma for precise immunotherapy and chemotherapy.Frontiers in immunology · 2022Article
- Benzyl and phenethyl isothiocyanates as promising epigenetic drug compounds by modulating histone acetylation and methylation marks in malignant melanoma.Investigational new drugs · 2021Article
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Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundHistone deacetylase (HDAC) inhibitors are widely used in clinical investigation as novel drug targets. For example, panobinostat and vorinostat have been used to treat patients with melanoma. However, HDAC inhibitors are small-molecule compounds without a specific target, and their mechanism of action is unclear. Therefore, it is necessary to investigate which HDACs are required for the proliferation and metastasis of melanoma cells.
methodsWe used overexpression and knocking down lentivirus to clarify the influence of HDAC5 and HDAC6 in melanoma development. Also, we introduced stable HDAC5 or HDAC6 knockdown cells into null mice and found that the knockdown cells were unable to form solid tumors. Finally, we tested HDAC5 and HDAC6 expression and sub-location in clinical melanoma tissues and tumor adjacent tissues.
resultsIn this study, and found that HDAC5 and HDAC6 were highly expressed in melanoma cells but exhibited low expression levels in normal skin cells. Furthermore, we knocked down HDAC5 or HDAC6 in A375 cells and demonstrated that both HDAC5 and HDAC6 contributed to the proliferation and metastasis of melanoma cells.
conclusionsThis study demonstrated both HDAC5 and HDAC6 were required for melanoma cell proliferation and metastasis through different signaling pathways.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.