ArticleJournal of cellular and molecular medicine2009
The histone deacetylase inhibitor valproic acid alters growth properties of renal cell carcinoma in vitro and in vivo.
Article in Journal of cellular and molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 56 citations in OpenAlex.
- Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Article
- The roles of histone deacetylases in kidney development and disease.Clinical and experimental nephrology · 2021Review
- Article
- Histone deacetylase inhibitors dysregulate DNA repair proteins and antagonize metastasis-associated processes.Journal of cancer research and clinical oncology · 2020Article
- Targeting the Immune system and Epigenetic Landscape of Urological Tumors.International journal of molecular sciences · 2020Review
- Histone deacetylase inhibitors differentially regulate c-Myc expression in retinoblastoma cells.Oncology letters · 2020Article
- Modulation of phospho-proteins by interferon-alpha and valproic acid in acute myeloid leukemia.Journal of cancer research and clinical oncology · 2019Article
- Simvastatin reduces the carcinogenic effect of 3-methylcholanthrene in renal epithelial cells through histone deacetylase 1 inhibition and RhoA reactivation.Scientific reports · 2019Article
- Histone Deacetylases and Histone Deacetylase Inhibitors: Molecular Mechanisms of Action in Various Cancers.Advanced biomedical research · 2019Review
- Combined Treatment with Valproic Acid and 5-Aza-2'-Deoxycytidine Synergistically Inhibits Human Clear Cell Renal Cell Carcinoma Growth and Migration.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- HDAC inhibition as a treatment concept to combat temsirolimus-resistant bladder cancer cells.Oncotarget · 2017Article
- Epigenome Aberrations: Emerging Driving Factors of the Clear Cell Renal Cell Carcinoma.International journal of molecular sciences · 2017Review
- Oxidative stress-induced epigenetic changes associated with malignant transformation of human kidney epithelial cells.Oncotarget · 2017Article
- Article
- The epigenetic landscape of clear-cell renal cell carcinoma.Journal of kidney cancer and VHL · 2015Article
- Molecular and immunologic markers of kidney cancer-potential applications in predictive, preventive and personalized medicine.The EPMA journal · 2015Review
- Harnessing the p53-PUMA axis to overcome DNA damage resistance in renal cell carcinoma.Neoplasia (New York, N.Y.) · 2014Article
- HDAC-inhibition counteracts everolimus resistance in renal cell carcinoma in vitro by diminishing cdk2 and cyclin A.Molecular cancer · 2014Article
- HDAC inhibitors in kidney development and disease.Pediatric nephrology (Berlin, Germany) · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylase (HDAC) inhibitors represent a promising class of antineoplastic agents which affect tumour growth, differentiation and invasion. The effects of the HDAC inhibitor valproic acid (VPA) were tested in vitro and in vivo on pre-clinical renal cell carcinoma (RCC) models. Caki-1, KTC-26 or A498 cells were treated with various concentrations of VPA during in vitro cell proliferation 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays and to evaluate cell cycle manipulation. In vivo tumour growth was conducted in subcutaneous xenograft mouse models. The anti-tumoural potential of VPA combined with low-dosed interferon-alpha (IFN-alpha) was also investigated. VPA significantly and dose-dependently up-regulated histones H3 and H4 acetylation and caused growth arrest in RCC cells. VPA altered cell cycle regulating proteins, in particular CDK2, cyclin B, cyclin D3, p21 and Rb. In vivo, VPA significantly inhibited the growth of Caki-1 in subcutaneous xenografts, accompanied by a strong accumulation of p21 and bax in tissue specimens of VPA-treated animals. VPA-IFN-alpha combination markedly enhanced the effects of VPA monotherapy on RCC proliferation in vitro, but did not further enhance the anti-tumoural potential of VPA in vivo. VPA was found to have profound effects on RCC cell growth, lending support to the initiation of clinical testing of VPA for treating advanced RCC.
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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.