ArticleOncotarget2017
Histone deacetylase inhibitors vorinostat and panobinostat induce G1 cell cycle arrest and apoptosis in multidrug resistant sarcoma cell lines.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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The trial behind it
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Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
- Review
- From Bench to Bedside: Advancements in Precision Oncology and Drug Discovery for Osteosarcoma.Cancers · 2026Review
- Panobinostat Potentiates the Antitumor Efficacy of 5-Fluorouracil in Gastric Cancer by Suppressing Thymidylate Synthase Expression.International journal of molecular sciences · 2026Article
- HIV-1 accessory protein Vpr possesses a cryptic p300-dependent transcription-promoting activity that is blocked by histone deacetylases in CD4+ T cells.PLoS pathogens · 2025Article
- Establishment and characterization of a novel patient-derived cell line from conventional central grade 3 chondrosarcoma, NCC-CS1-C1.Human cell · 2024Article
- High-Throughput Drug Screening in Chondrosarcoma Cells Identifies Effective Antineoplastic Agents Independent of IDH Mutation.International journal of molecular sciences · 2024Article
- The thiol methyltransferase activity of TMT1A (METTL7A) is conserved across species.Chemico-biological interactions · 2024Article
- The Methyltransferases METTL7A and METTL7B Confer Resistance to Thiol-Based Histone Deacetylase Inhibitors.Molecular cancer therapeutics · 2024Article
- Gesicles packaging dCas9-VPR ribonucleoprotein complexes can combine with vorinostat and promote HIV proviral transcription.Molecular therapy. Methods & clinical development · 2024Article
- The thiol methyltransferase activity of TMT1A (METTL7A) is conserved across species.bioRxiv : the preprint server for biology · 2023Article
- Targeting the Clear Cell Sarcoma Oncogenic Driver Fusion GeneCancer research communications · 2023Article
- Exploring the Potential of Phytocompounds for Targeting Epigenetic Mechanisms in Rheumatoid Arthritis: An In Silico Study Using Similarity Indexing.Molecules (Basel, Switzerland) · 2023Article
- BMX, a specific HDAC8 inhibitor, with TMZ for advanced CRC therapy: a novel synergic effect to elicit p53-, β-catenin- and MGMT-dependent apoptotic cell death.Cell communication and signaling : CCS · 2022Article
- Image-Based Annotation of Chemogenomic Libraries for Phenotypic Screening.Molecules (Basel, Switzerland) · 2022Article
- Systemic Therapy for Chondrosarcoma.Current treatment options in oncology · 2022Review
- Lysosome activable polymeric vorinostat encapsulating PD-L1KD for a combination of HDACi and immunotherapy.Drug delivery · 2021Article
- Growth Inhibition and Induction of Innate Immune Signaling of Chondrosarcomas with Epigenetic Inhibitors.Molecular cancer therapeutics · 2021Article
- The Effect of Organoselenium Compounds on Histone Deacetylase Inhibition and Their Potential for Cancer Therapy.International journal of molecular sciences · 2021Review
- Deacetylation of Transcription Factors in Carcinogenesis.International journal of molecular sciences · 2021Review
- Evaluation of histone deacetylase inhibitor substituted zinc and indium phthalocyanines for chemo- and photodynamic therapy.RSC advances · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synovial sarcoma and high grade chondrosarcoma are characterized by their lack of response to conventional cytotoxic chemotherapy, the tendency to develop lung metastases, and low survival rates. Research within the field prioritizes the development and expansion of new treatment options for dealing with unresectable or metastatic diseases. Numerous clinical trials using histone deacetylases inhibitors (HDACi) have shown specific efficacy as an active antitumor agent for treating a variety of solid tumors. However, as of yet the effect of different HDACi on synovial- and chondrosarcoma cells has not been investigated. In this study, vorinostat (SAHA), panobinostat (LBH-589), and belinostat (PXD101) decreased cell viability of synovial sarcoma (SW-982) and chondrosarcoma (SW-1353) cells in a time- and dose dependent manner and arrested SW-982 cells in the G1/S phase. Western blot analysis determined the responsible cell cycle regulator proteins. In addition, we found apoptotic induction by caspase 3/7 activity, caspase 3 cleavage, and PARP cleavage. In SW-1353 cells only SAHA showed comparable effects. Noteworthy, all HDACi tested had synergistic effects with the topoisomerase II inhibitor doxorubicin in SW-1353 chondrosarcoma cells making the cells more sensitive to the chemotherapeutic drug. Our results show for the first time that SAHA and LBH-589 reduced viability of sarcoma cells and arrested them at the G1/S checkpoint, while also inducing apoptosis and enhancing chemotherapeutic sensitivity, especially in chondrosarcoma cells. These data demonstrate the exciting potential of HDACi for use in sarcoma treatment.
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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.