ArticleCancer management and research2018
CDK7 inhibition is a novel therapeutic strategy against GBM both in vitro and in vivo.
Article in Cancer management and research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Bibliometric analysis of evolutionary trends and hotspots of super-enhancers in cancer.Frontiers in pharmacology · 2023Pooled it
- CDK12/CDK13 inhibition disrupts transcriptional elongation and replication fork progression in glioblastoma.EMBO molecular medicine · 2026Article
- CDK12 regulates cellular metabolism to promote glioblastoma growth.JCI insight · 2025Article
- CDK7 inhibition promotes glioblastoma cell death through convergent transcriptional and metabolic stress pathways.Clinical and translational medicine · 2025Article
- Epigenetic Alterations in Glioblastoma Multiforme as Novel Therapeutic Targets: A Scoping Review.International journal of molecular sciences · 2025Article
- Super-enhancers in immune system regulation: mechanisms, pathological reprogramming, and therapeutic opportunities.Frontiers in immunology · 2025Review
- Super-enhancer inhibitors THZ2 and JQ1 reverse temozolomide resistance in glioblastoma by suppressing SE-driven SOX9 expression.Cancer drug resistance (Alhambra, Calif.) · 2025Article
- CDK7 in breast cancer: mechanisms of action and therapeutic potential.Cell communication and signaling : CCS · 2024Review
- Super-Enhancers and Their Parts: From Prediction Efforts to Pathognomonic Status.International journal of molecular sciences · 2024Review
- CDK7 and CDK9 inhibition interferes with transcription, translation, and stemness, and induces cytotoxicity in GBM irrespective of temozolomide sensitivity.Neuro-oncology · 2024Article
- Multi-Target Neural Differentiation (MTND) Therapeutic Cocktail to Suppress Brain Tumor.International journal of molecular sciences · 2023Article
- Super-enhancers complexes zoom in transcription in cancer.Journal of experimental & clinical cancer research : CR · 2023Review
- Article
- Superenhancers as master gene regulators and novel therapeutic targets in brain tumors.Experimental & molecular medicine · 2023Review
- Targeting pre-mRNA splicing in cancers: roles, inhibitors, and therapeutic opportunities.Frontiers in oncology · 2023Review
- Widespread hypertranscription in aggressive human cancers.Science advances · 2022Article
- Blocking CDK7-Mediated NOTCH1-cMYC Signaling Attenuates Cancer Stem Cell Activity in Anaplastic Thyroid Cancer.Thyroid : official journal of the American Thyroid Association · 2022Article
- Identification of Four Enhancer-Associated Genes as Risk Signature for Diffuse Glioma Patients.Journal of molecular neuroscience : MN · 2022Article
- Oncogenic dysregulation of pre-mRNA processing by protein kinases: challenges and therapeutic opportunities.The FEBS journal · 2021Review
- Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGlioblastoma multiforme (GBM) remains to be one of the top lethal cancer types for adult to date. Current GBM therapies suffer greatly from the highly heterogeneous and adaptable nature of GBM cells, indicating an urgent need of alternative therapeutic options. In this study, we focused on identifying novel epigenetic targeted strategy against GBM.
methodsA collection of epigenetic modulating small molecules were subjected to anti-GBM screening and the inhibitory effect of identified agent was validated both in vitro and in vivo. Genetic targeting approaches were also used to verify the on-target inhibitory effect of identified agent. Furthermore, the inhibitory mechanism of identified agent was investigated by integrative analyses of drug-treated GBM cells and GBM tumor databases.
resultsThe covalent CDK7 inhibitor THZ1 was one of the top hits in our screening and its anti-GBM activity was confirmed both in vitro and in vivo. CDK7 inhibition through CRISPR-Cas9 or RNA interference also markedly disrupted GBM cell growth. Furthermore, analyses of multiple GBM tumor databases consistently revealed that CDK7 expression was significantly elevated in GBM compared with normal brain tissues and lower grade gliomas. Higher CDK7 expression was correlated with worse prognosis for both glioma and GBM. Mechanistically, THZ1 treatment led to considerable disruption of global gene transcription in GBM cells, preferentially targeting those associated with super-enhancers (SEs). We also showed that THZ1 sensitive and SE-related genes had important roles for GBM growth.
conclusionOur study shows that targeting SE-associated transcription addiction by CDK7 inhibition could be an effective therapeutic strategy against GBM.
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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.