ArticleCell death & disease2021
HDAC4 promotes nasopharyngeal carcinoma progression and serves as a therapeutic target.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 48 citations in OpenAlex.
- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
- An HDAC4-specific PROTAC degrader achieves radiation sensitization by enhancing ferroptosis in lung cancer.Nature communications · 2026Article
- Epigenetics: the master switch of nasopharyngeal carcinoma invasion and metastasis.Frontiers in immunology · 2026Review
- CircPPP1CB subtype, hsa_circ_0007439, promotes nasopharyngeal carcinoma progression by upregulating KRT1.Discover oncology · 2025Article
- Article
- Glucocorticoids regulate the expression of Srsf1 through Hdac4/Foxc1 axis to induce apoptosis of osteoblasts.Communications biology · 2025Article
- Role of N6-methyladenosine methylation in nasopharyngeal carcinoma: current insights and future prospective.Cell death discovery · 2024Review
- The role of circular RNA targeting IGF2BPs in cancer-a potential target for cancer therapy.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Circulating tumor cells: from new biological insights to clinical practice.Signal transduction and targeted therapy · 2024Review
- Article
- HDAC6-mediated deacetylation of FLOT2 maintains stability and tumorigenic function of FLOT2 in nasopharyngeal carcinoma.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Article
- Targeting histone deacetylases in head and neck squamous cell carcinoma: molecular mechanisms and therapeutic targets.Journal of translational medicine · 2024Review
- Associations in cell type-specific hydroxymethylation and transcriptional alterations of pediatric central nervous system tumors.Nature communications · 2024Article
- Oncogenic and immunological roles of RACGAP1 in pan-cancer and its potential value in nasopharyngeal carcinoma.Apoptosis : an international journal on programmed cell death · 2024Article
- Epigenetic regulation in cancer.MedComm · 2024Review
- Qingrexiaoji Recipe Regulates the Differentiation of M2 TAMCombinatorial chemistry & high throughput screening · 2024Article
- Ginsenoside Rh4 inhibits inflammation-related hepatocellular carcinoma progression by targeting HDAC4/IL-6/STAT3 signaling.Molecular genetics and genomics : MGG · 2023Article
- Identification of HDAC4 as a potential therapeutic target and prognostic biomarker for ZFTA-fused ependymomas.Cancer gene therapy · 2023Article
- Synergistic Interaction of the Class IIa HDAC Inhibitor CHDI0039 with Bortezomib in Head and Neck Cancer Cells.International journal of molecular sciences · 2023Article
- Hydroxymethylation alterations in progenitor-like cell types of pediatric central nervous system tumors are associated with cell type-specific transcriptional changes.Research square · 2023Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylases (HDACs) are involved in tumor progression, and some have been successfully targeted for cancer therapy. The expression of histone deacetylase 4 (HDAC4), a class IIa HDAC, was upregulated in our previous microarray screen. However, the role of HDAC4 dysregulation and mechanisms underlying tumor growth and metastasis in nasopharyngeal carcinoma (NPC) remain elusive. Here, we first confirmed that the HDAC4 levels in primary and metastatic NPC tissues were significantly increased compared with those in normal nasopharyngeal epithelial tissues and found that high HDAC4 expression predicted a poor overall survival (OS) and progression-free survival (PFS). Functionally, HDAC4 accelerated cell cycle G1/S transition and induced the epithelial-to-mesenchymal transition to promote NPC cell proliferation, migration, and invasion in vitro, as well as tumor growth and lung metastasis in vivo. Intriguingly, knockdown of N-CoR abolished the effects of HDAC4 on the invasion and migration abilities of NPC cells. Mechanistically, HDAC3/4 binds to the E-cadherin promoter to repress E-cadherin transcription. We also showed that the HDAC4 inhibitor tasquinimod suppresses tumor growth in NPC. Thus, HDAC4 may be a potential diagnostic marker and therapeutic target in patients with NPC.
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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.