ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014
Down-regulation of HDAC5 inhibits growth of human hepatocellular carcinoma by induction of apoptosis and cell cycle arrest.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- The prognosis and clinicopathological significance of histone deacetylase in hepatocellular carcinoma: a meta-analysis.Clinical and experimental medicine · 2023Pooled it
- Whole Exome Sequencing IdentifiesInternational journal of molecular sciences · 2021Trial
- Histone deacetylases: Function in tumor development and therapeutic prospects (Review).Oncology letters · 2026Review
- Targeting glioblastoma with HDAC inhibitors: insights into hydroxamic acid-based therapeutic strategies.Acta neuropathologica communications · 2025Article
- Review
- Recent Advancements in the Development of HDAC/Tubulin Dual-Targeting Inhibitors.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Acetylation of E2F1 at K125 facilitates cell apoptosis under serum stress.Translational oncology · 2025Article
- Mechanisms of HDACs in cancer development.Frontiers in immunology · 2025Review
- Sodium valproate affects the expression of p16Oncology letters · 2024Article
- The therapeutic potential of targeting the CHD protein family in cancer.Pharmacology & therapeutics · 2024Review
- Comprehensive Analysis of the Prognostic Implications and Biological Function of HDACs in Liver Hepatocellular Carcinoma.International journal of medical sciences · 2024Article
- Targeting histone deacetylases for cancer therapy: Trends and challenges.Acta pharmaceutica Sinica. B · 2023Review
- HighAnnals of translational medicine · 2022Article
- Histone deacetylase (HDAC) 11 inhibits matrix metalloproteinase (MMP) 3 expression to suppress colorectal cancer metastasis.Journal of Cancer · 2022Article
- Crosstalk between Statins and Cancer Prevention and Therapy: An Update.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Review
- Unraveling the Epigenetic Role and Clinical Impact of Histone Deacetylases in Neoplasia.Diagnostics (Basel, Switzerland) · 2021Review
- Characterization of Histone Deacetylase Mechanisms in Cancer Development.Frontiers in oncology · 2021Review
- Insights Into the Function and Clinical Application of HDAC5 in Cancer Management.Frontiers in oncology · 2021Review
- Promoter Hypomethylation and miR-145-5p Downregulation- Mediated HDAC11 Overexpression Promotes Sorafenib Resistance and Metastasis of Hepatocellular Carcinoma Cells.Frontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylases (HDACs) play a critical role in the proliferation, differentiation, and apoptosis of cancer cells. An obstacle for the application of HDAC inhibitors as effective anti-cancer therapeutics is that our current knowledge on the contributions of different HDACs in various cancer types remains scarce. The present study reported that the mRNA and protein levels of HDAC5 were up-regulated in human hepatocellular carcinoma (HCC) tissues and cells as shown by quantitative real-time PCR and Western blot. MTT assay and BrdU incorporation assay showed that the down-regulation of HDAC5 inhibited cell proliferation in HepG2, Hep3B, and Huh7 cell lines. Data from in vivo xenograft tumorigenesis model also demonstrated the anti-proliferative effect of HDAC5 depletion on tumor cell growth. Furthermore, the suppression of HDAC5 promoted cell apoptosis and induced G1-phase cell cycle arrest in HCC cells. On the molecular level, we observed altered expression of apoptosis-related proteins such as p53, bax, bcl-2, cyto C, and caspase 3 in HDAC5-shRNA-transfected cells. Knockdown of HDAC5 led to a significant up-regulation of p21 and down-regulation of cyclin D1 and CDK2/4/6. We also found that the down-regulation of HDAC5 substantially increased p53 stability and promoted its nuclear localization and transcriptional activity. Our study suggested that knockdown of HDAC5 could inhibit cancer cell proliferation by the induction of cell cycle arrest and apoptosis; thus, suppression of HDAC5 may be a viable option for treating HCC patients.
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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.