ArticleMolecular biology reports2014
VPA inhibits renal cancer cell migration by targeting HDAC2 and down-regulating HIF-1α.
Article in Molecular biology reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Macrophage metabolic reprogramming via HIF-1α-glycolysis drives osteoblast ferroptosis and bone loss through an IL-6-STAT3-dependent redox axis.Redox report : communications in free radical research · 2026Article
- Lactylation in kidney diseases: a review of regulatory mechanisms and therapeutic prospects.Frontiers in cell and developmental biology · 2026Review
- Histone deacetylases and their inhibitors in kidney diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Acetylation increases expression, interaction with TRAPPC4 and surface localization of PD-L1.Discover oncology · 2023Article
- Integrated metabolism and epigenetic modifications in the macrophages of mice in responses to cold stress.Journal of Zhejiang University. Science. B · 2022Article
- Decoding molecular recognition of inhibitors targeting HDAC2 via molecular dynamics simulations and configurational entropy estimation.PloS one · 2022Article
- Histone deacetylase‑2: A potential regulator and therapeutic target in liver disease (Review).International journal of molecular medicine · 2021Review
- Valproic Acid: A Promising Therapeutic Agent in Glioma Treatment.Frontiers in oncology · 2021Review
- Apoptosis Induction byHistone Deacetylase Inhibitors in Cancer Cells: Role of Ku70.International journal of molecular sciences · 2019Review
- Valproic acid inhibits the angiogenic potential of cervical cancer cells via HIF-1α/VEGF signals.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2016Article
- Overexpression screens identify conserved dosage chromosome instability genes in yeast and human cancer.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Class I and IIa HDACs Mediate HIF-1α Stability Through PHD2-Dependent Mechanism, While HDAC6, a Class IIb Member, Promotes HIF-1α Transcriptional Activity in Nucleus Pulposus Cells of the Intervertebral Disc.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2016Article
- Development, Maintenance, and Reversal of Multiple Drug Resistance: At the Crossroads of TFPI1, ABC Transporters, and HIF1.Cancers · 2015Review
- Article
- Histone deacetylase inhibitor valproic acid (VPA) promotes the epithelial mesenchymal transition of colorectal cancer cells via up regulation of Snail.Cell adhesion & migration · 2015Article
- Pharmacologically relevant doses of valproate upregulate CD20 expression in three diffuse large B-cell lymphoma patients in vivo.Experimental hematology & oncology · 2015Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell migration plays major roles in human renal cancer-related death, but the molecular mechanisms remain unclear. Valproic acid (VPA) is a broad-spectrum inhibitor of class I and II histone deacetylases and shows great anticancer activity in a variety of human cancers. In this study, we found that VPA significantly inhibited cell migration but not proliferation of human renal cancer ACHN cells. Mechanistic studies found that VPA significantly inhibited the expression of HIF-1α. Knockdown of HIF-1α could obviously inhibited cell migration, while over-expression of HIF-1α markedly rescued the inhibition of VPA on cell migration. Further studies found that knockdown of HDAC2 completely mimicked the effects of VPA on HIF-1α and cell migration, and over-expression of HIF-1α could also rescue the effects of HDAC2 knockdown on cell migration. Collectively, these results indicated that the potential of specific inhibition of HDAC2 by small molecular chemicals may lead to future therapeutic agents in human renal cancer treatment.
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