ArticleMolecular cancer therapeutics2016
The Bromodomain BET Inhibitor JQ1 Suppresses Tumor Angiogenesis in Models of Childhood Sarcoma.
Article in Molecular cancer therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.
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- Computational discovery of BRD4 inhibitors for neuroblastoma therapy using pharmacophore screening and molecular simulations.Scientific reports · 2025Article
- Simultaneous inhibition of TRIM24 and TRIM28 sensitises prostate cancer cells to antiandrogen therapy, decreasing VEGF signalling and angiogenesis.Molecular oncology · 2025Article
- A heterodimer of hemoglobin identifies theranostic targets on brain-metastasizing melanoma cells.International journal of cancer · 2025Article
- Functional combinatorial precision medicine for predicting and optimizing soft tissue sarcoma treatments.NPJ precision oncology · 2025Article
- Epigenetic regulation of angiogenesis and its therapeutics.Genomics & informatics · 2025Review
- Characterization and Experimental Use of Multiple Myeloma Bone Marrow Endothelial Cells and Progenitors.International journal of molecular sciences · 2024Article
- Investigation of the impact of bromodomain inhibition on cytoskeleton stability and contraction.Cell communication and signaling : CCS · 2024Article
- BRD4 isoforms have distinct roles in tumour progression and metastasis in rhabdomyosarcoma.EMBO reports · 2024Article
- Establishment and functional testing of a novel ex vivo extraskeletal osteosarcoma cell model (USZ20-ESOS1).Human cell · 2024Article
- Investigation of the impact of bromodomain inhibition on cytoskeleton stability and contraction.bioRxiv : the preprint server for biology · 2023Article
- Pyronaridine as a Bromodomain-Containing Protein 4-Molecules (Basel, Switzerland) · 2023Article
- Molecular Subtypes and Tumor Microenvironment Characteristics of Small-Cell Lung Cancer Associated with Platinum-Resistance.Cancers · 2023Article
- Redundant Signaling as the Predominant Mechanism for Resistance to Antibodies Targeting the Type-I Insulin-Like Growth Factor Receptor in Cells Derived from Childhood Sarcoma.Molecular cancer therapeutics · 2023Article
- BET Bromodomain Degradation Disrupts Function but Not 3D Formation of RNA Pol2 Clusters.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Ewing Sarcoma Meets Epigenetics, Immunology and Nanomedicine: Moving Forward into Novel Therapeutic Strategies.Cancers · 2022Review
- Small Molecule BRD4 Inhibitors Apabetalone and JQ1 Rescues Endothelial Cells Dysfunction, Protects Monolayer Integrity and Reduces Midkine Expression.Molecules (Basel, Switzerland) · 2022Article
- Combined inhibition of BET bromodomain and mTORC1/2 provides therapeutic advantage for rhabdomyosarcoma by switching cell death mechanism.Molecular carcinogenesis · 2022Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
The bromodomain and extra-terminal domain inhibitor JQ1 has marked antitumor activity against several hematologic malignancies as well as solid tumor models. Here, we investigated its activity in vitro and in vivo against models of childhood rhabdomyosarcoma and Ewing sarcoma. In vitro, JQ1 (but not the inactive enantiomer JQ1R) inhibited cell proliferation and increased G1 fraction of cells, although there was no correlation between cell line sensitivity and suppression of c-MYC or MYCN. In vivo, xenografts showed significant inhibition of growth during the period of treatment, and rapid regrowth after treatment was stopped, activity typical of antiangiogenic agents. Furthermore, xenografts derived from cell lines intrinsically resistant or sensitive to JQ1 in vitro had similar sensitivity in vivo as xenografts. Further investigation showed that JQ1 reduced tumor vascularization. This was secondary to both drug-induced downregulation of tumor-derived growth factors and direct effects of JQ1 on vascular elements. JQ1 suppressed VEGF-stimulated vascularization of Matrigel plugs in mice, and in vitro suppressed differentiation, proliferation, and invasion of human umbilical cord vascular endothelial cells (HUVEC). In HUVECs, JQ1 partially suppressed c-MYC levels, but dramatically reduced AP-1 levels and activity through suppression of the AP-1-associated protein FOSL1. Our data suggest that the antitumor activity of JQ1 in these sarcoma models is largely a consequence of its antiangiogenic activity. Mol Cancer Ther; 15(5); 1018-28. ©2016 AACR.
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