ArticleCancers2022
Selective CDK9 Inhibition by Natural Compound Toyocamycin in Cancer Cells.
Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
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- BRD4 acts as a transcriptional repressor of RhoB to inhibit terminal erythropoiesis.Journal of hematology & oncology · 2025Article
- Endoplasmic Reticulum Stress in Acute Myeloid Leukemia: Pathogenesis, Prognostic Implications, and Therapeutic Strategies.International journal of molecular sciences · 2025Review
- ADCY5 Gene Affects Seasonal Reproduction in Dairy Goats by Regulating Ovarian Granulosa Cells Steroid Hormone Synthesis.International journal of molecular sciences · 2025Article
- Endoplasmic reticulum stress in lung cancer.Frontiers in oncology · 2025Review
- NRGSuite-Qt: a PyMOL plugin for high-throughput virtual screening, molecular docking, normal-mode analysis, the study of molecular interactions, and the detection of binding-site similarities.Bioinformatics advances · 2025Article
- CdgB Regulates Morphological Differentiation and Toyocamycin Production inInternational journal of molecular sciences · 2024Article
- MC180295 is a highly potent and selective CDK9 inhibitor with preclinical in vitro and in vivo efficacy in cancer.Clinical epigenetics · 2024Article
- Metabolic perturbation ofFrontiers in microbiology · 2024Article
- The Oncogenic Protein Kinase/ATPase RIOK1 Is Up-Regulated via the c-myc/E2F Transcription Factor Axis in Prostate Cancer.The American journal of pathology · 2023Article
- Multifunctional nanomedicines-enabled chemodynamic-synergized multimodal tumor therapy via Fenton and Fenton-like reactions.Theranostics · 2023Review
- Epigenetic Mechanisms Underlying Melanoma Resistance to Immune and Targeted Therapies.Cancers · 2022Review
- WXJ-202, a novel Ribociclib derivative, exerts antitumor effects against breast cancer through CDK4/6.Frontiers in pharmacology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 7 institutions in 2 countries.
Funding
Abstract
Aberrant transcription in cancer cells involves the silencing of tumor suppressor genes (TSGs) and activation of oncogenes. Transcriptomic changes are associated with epigenomic alterations such as DNA-hypermethylation, histone deacetylation, and chromatin condensation in promoter regions of silenced TSGs. To discover novel drugs that trigger TSG reactivation in cancer cells, we used a GFP-reporter system whose expression is silenced by promoter DNA hypermethylation and histone deacetylation. After screening a natural product drug library, we identified that toyocamycin, an adenosine-analog, induces potent GFP reactivation and loss of clonogenicity in human colon cancer cells. Connectivity-mapping analysis revealed that toyocamycin produces a pharmacological signature mimicking cyclin-dependent kinase (CDK) inhibitors. RNA-sequencing revealed that the toyocamycin transcriptomic signature resembles that of a specific CDK9 inhibitor (HH1). Specific inhibition of RNA Pol II phosphorylation level and kinase assays confirmed that toyocamycin specifically inhibits CDK9 (IC
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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.