ArticleNature communications2020
Selective inhibition of cancer cell self-renewal through a Quisinostat-histone H1.0 axis.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
19 citing papers in PubMed, 45 citations in OpenAlex.
- Neofunctionalization of H1 linker histones drives divergent gene expression and histone methylation in Cryptococcus neoformans.Communications biology · 2026Article
- TRIM21 promotes astrocyte-mediated neuroinflammation in experimental autoimmune encephalomyelitis by stabilizing RGMa via K33-linked ubiquitination.Journal of neuroinflammation · 2026Article
- Epigenetic potentiation of 5-fluorouracil by HDAC inhibitor quisinostat enhances antitumor effects in colorectal cancer.Cancer cell international · 2025Article
- A propidium iodide-basedAntimicrobial agents and chemotherapy · 2025Article
- H1-0 is a specific mediator of the repressive ETV6::RUNX1 transcriptional landscape in preleukemia and B cell acute lymphoblastic leukemia.HemaSphere · 2025Article
- PerturBase: a comprehensive database for single-cell perturbation data analysis and visualization.Nucleic acids research · 2025Article
- Utilizing epigenetic regulators to improve HSC-based lentiviral gene therapy.Blood advances · 2024Article
- Review
- Molecular, Cellular, and Technical Aspects of Breast Cancer Cell Lines as a Foundational Tool in Cancer Research.Life (Basel, Switzerland) · 2023Review
- The Way to Malignant Transformation: Can Epigenetic Alterations Be Used to Diagnose Early-Stage Head and Neck Cancer?Biomedicines · 2023Review
- Nanoconjugated long non-coding RNA MEG3 as a new therapeutic approach for Hepatocellular carcinoma.Heliyon · 2023Article
- Pharmaceutical Reactivation of Attenuated Apoptotic Pathways Leads to Elimination of Osimertinib Drug-Tolerant Cells.Cancer research communications · 2022Article
- Combining histone deacetylase inhibitors (HDACis) with other therapies for cancer therapy.European journal of medicinal chemistry · 2021Review
- Antimalarial Inhibitors Targeting Epigenetics or Mitochondria inMolecules (Basel, Switzerland) · 2021Review
- Disruption of the MSL complex inhibits tumour maintenance by exacerbating chromosomal instability.Nature cell biology · 2021Article
- Role of Plant-Derived Natural Compounds in Experimental Autoimmune Encephalomyelitis: A Review of the Treatment Potential and Development Strategy.Frontiers in pharmacology · 2021Review
- Novel targeted therapies of T cell lymphomas.Journal of hematology & oncology · 2020Review
- CD13 promotes hepatocellular carcinogenesis and sorafenib resistance by activating HDAC5-LSD1-NF-κB oncogenic signaling.Clinical and translational medicine · 2020Article
- Label-Free Mass Spectrometry-Based Quantification of Linker Histone H1 Variants in Clinical Samples.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
Abstract
Continuous cancer growth is driven by subsets of self-renewing malignant cells. Targeting of uncontrolled self-renewal through inhibition of stem cell-related signaling pathways has proven challenging. Here, we show that cancer cells can be selectively deprived of self-renewal ability by interfering with their epigenetic state. Re-expression of histone H1.0, a tumor-suppressive factor that inhibits cancer cell self-renewal in many cancer types, can be broadly induced by the clinically well-tolerated compound Quisinostat. Through H1.0, Quisinostat inhibits cancer cell self-renewal and halts tumor maintenance without affecting normal stem cell function. Quisinostat also hinders expansion of cells surviving targeted therapy, independently of the cancer types and the resistance mechanism, and inhibits disease relapse in mouse models of lung cancer. Our results identify H1.0 as a major mediator of Quisinostat's antitumor effect and suggest that sequential administration of targeted therapy and Quisinostat may be a broadly applicable strategy to induce a prolonged response in patients.
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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.