ArticleWorld journal of urology2011
Alterations of the gene expression profile in renal cell carcinoma after treatment with the histone deacetylase-inhibitor valproic acid and interferon-alpha.
Article in World journal of urology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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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
9 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Role of Chemokine Receptor CXCR3 and Its Ligands in Renal Cell Carcinoma.International journal of molecular sciences · 2020Pooled it
- Comprehensive Analysis of Transcriptomic Profiles Identified the Prediction of Prognosis and Drug Sensitivity of Aminopeptidase-Like 1 (NPEPL1) for Clear Cell Renal Cell Carcinoma.Journal of oncology · 2023Article
- Targeting the Immune system and Epigenetic Landscape of Urological Tumors.International journal of molecular sciences · 2020Review
- Regulation of Chemokines and Cytokines by Histone Deacetylases and an Update on Histone Decetylase Inhibitors in Human Diseases.International journal of molecular sciences · 2019Review
- Molecular and immunologic markers of kidney cancer-potential applications in predictive, preventive and personalized medicine.The EPMA journal · 2015Review
- Tumor Growth Mitigating Effects of Valproic Acid in Systemic Malignancies.Journal of thyroid research · 2015Article
- Cross-communication between histone H3 and H4 acetylation and Akt-mTOR signalling in prostate cancer cells.Journal of cellular and molecular medicine · 2014Article
- Integrin α7 binds tissue inhibitor of metalloproteinase 3 to suppress growth of prostate cancer cells.The American journal of pathology · 2013Article
- Selection of reference genes for use in quantitative reverse transcription PCR assays when using interferons in U87MG.Molecular biology reports · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeRenal cell carcinoma (RCC) is highly resistant to chemotherapy and unresponsive to radio- and immunotherapy. Recently, we have documented that the histone deacetylase (HDAC)-inhibitor valproic acid (VPA) in combination with low-dosed interferon (IFN)-alpha significantly inhibits RCC proliferation and adhesion in vitro and in vivo. The current study investigated the effects of these compounds on gene transcription of metastatic RCC cell line Caki-1 after 3 and 5 days exposure.
methodsTo evaluate the gene expression profiles of the RCC cells, we performed microarray analysis using Affymetrix GeneChip. Selected significant genes were further validated by Real Time PCR.
resultsMicroarray revealed that VPA altered genes that are involved in cell growth, cell survival, immune response, cell motility and cell adhesion. Combination of VPA with IFN-alpha not only enhanced the effects on gene transcription but also resulted in the expression of novel genes, which were not induced by either VPA or IFN-alpha alone. Among the up-regulated genes were chemokines (CXCL10, CXCL11, CXCL16) and integrins (ITGA2, ITGA4, ITGA5, ITGA6, ITGA7). Genes encoding for adhesion molecules (NCAM1, ICAM1, VCAM1) were also modulated. Real Time PCR approved these findings.
conclusionThis data provides insight into the molecular mechanism of action of the combined treatment of VPA and IFN-alpha in RCC. Implications are that the combined application of VPA and IFN-alpha may represent a more efficient alternative to existing therapy options for RCC.
Indexed as
Identifiers
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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 Socratic graph.