ArticlePloS one2015
Molecular Mechanism of the Cell Death Induced by the Histone Deacetylase Pan Inhibitor LBH589 (Panobinostat) in Wilms Tumor Cells.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Gene signature associated with benign neurofibroma transformation to malignant peripheral nerve sheath tumors.PloS one · 2017Pooled it
- Modeling high-risk Wilms tumors enables the discovery of therapeutic vulnerability.Cell reports. Medicine · 2024Article
- HER3 targeting augments the efficacy of panobinostat in claudin-low triple-negative breast cancer cells.NPJ precision oncology · 2023Article
- Targeted Epigenetic Interventions in Cancer with an Emphasis on Pediatric Malignancies.Biomolecules · 2022Review
- Identification of repurposed drugs targeting significant long non-coding RNAs in the cross-talk between diabetes mellitus and Alzheimer's disease.Scientific reports · 2022Article
- Zap-Pano: a Photocaged Prodrug of the KDAC Inhibitor Panobinostat.ChemMedChem · 2021Article
- Synergistic Tumor Cytolysis by NK Cells in Combination With a Pan-HDAC Inhibitor, Panobinostat.Frontiers in immunology · 2021Article
- QuaDMutNetEx: a method for detecting cancer driver genes with low mutation frequency.BMC bioinformatics · 2020Article
- Proteomics analysis of fetal growth restriction and taurine‑treated fetal growth restriction rat brain tissue by 2D DIGE and MALDI‑TOF/TOF MS analysis.International journal of molecular medicine · 2019Article
- O-GlcNAc-induced nuclear translocation of hnRNP-K is associated with progression and metastasis of cholangiocarcinoma.Molecular oncology · 2019Article
- Molecular mechanism of GCancer cell international · 2017Article
- Downregulation of the long noncoding RNA GAS5-AS1 contributes to tumor metastasis in non-small cell lung cancer.Scientific reports · 2016Article
- Facile preparation of salivary extracellular vesicles for cancer proteomics.Scientific reports · 2016Article
- A novel sphingosine kinase 1 inhibitor (SKI-5C) induces cell death of Wilms' tumor cellsAmerican journal of translational research · 2016Article
- Andrographolide promotes vincristine-induced SK-NEP-1 tumor cell death via PI3K-AKT-p53 signaling pathway.Drug design, development and therapy · 2016Article
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Authors and funding
27 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWilms tumor (WT) is an embryonic kidney cancer, for which histone acetylation might be a therapeutic target. LBH589, a novel targeted agent, suppresses histone deacetylases in many tumors. This study investigated the antitumor activity of LBH589 in SK-NEP-1 and G401 cells.
methodsSK-NEP-1 and G401 cell growth was assessed by CCK-8 and in nude mice experiments. Annexin V/propidium iodide staining followed by flow cytometry detected apoptosis in cell culture. Gene expressions of LBH589-treated tumor cells were analyzed using an Arraystar Human LncRNA Array. The Multi Experiment View cluster software analyzed the expression data. Differentially expressed genes from the cluster analyses were imported into the Ingenuity Pathway Analysis tool.
resultsLBH589 inhibited cell proliferation of SK-NEP-1 and G401 cells in a dose-dependent manner. Annexin V, TUNEL and Hochest 33342 staining analysis showed that LBH589-treated cells showed more apoptotic features compared with the control. LBH589 treatment inhibited the growth of SK-NEP-1 xenograft tumors in nude mice. Arraystar Human LncRNA Array analysis of genes and lncRNAs regulated by LBH589 identified 6653 mRNAs and 8135 lncRNAs in LBH589-treated SK-NEP-1 cells. The most enriched gene ontology terms were those involved in nucleosome assembly. KEGG pathway analysis identified cell cycle proteins, including CCNA2, CCNB2, CCND1, CCND2, CDK4, CDKN1B and HDAC2, etc. Ingenuity Pathway Analysis identified important upstream molecules: HIST2H3C, HIST1H4A, HIST1A, HIST1C, HIST1D, histone H1, histone H3, RPRM, HSP70 and MYC.
conclusionsLBH589 treatment caused apoptosis and inhibition of cell proliferation of SK-NEP-1and G401 cells. LBH589 had a significant effect and few side effects on SK-NEP-1 xenograft tumors. Expression profiling, and GO, KEGG and IPA analyses identified new targets and a new "network" of genes responding to LBH589 treatment in SK-NEP-1 cells. RPRM, HSP70 and MYC may be important regulators during LBH589 treatment. Our results provide new clues to the proapoptotic mechanism of LBH589.
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