ArticleEMBO reports2021
CDK7 and MITF repress a transcription program involved in survival and drug tolerance in melanoma.
Article in EMBO reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- The Role of Transcriptional and Atypical Cyclin-Dependent Protein Kinases in Melanoma.Cancers · 2026Review
- STADiffuser: high-fidelity simulation and full-view 3D modeling of spatial transcriptomics.Nature communications · 2026Article
- Loss of MITF activity leads to emergent cell states from the melanocyte stem cell lineage.bioRxiv : the preprint server for biology · 2026Article
- Drug-induced tolerant persisters in tumor: mechanism, vulnerability and perspective implication for clinical treatment.Molecular cancer · 2025Review
- Pan-inhibition of super-enhancer-driven oncogenic transcription by next-generation synthetic ecteinascidins yields potent anti-cancer activity.Nature communications · 2025Article
- AMBRA1 levels predict resistance to MAPK inhibitors in melanoma.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Article
- BRAF Mutations in Melanoma: Biological Aspects, Therapeutic Implications, and Circulating Biomarkers.Cancers · 2023Review
- Quantitative landscapes reveal trajectories of cell-state transitions associated with drug resistance in melanoma.iScience · 2022Article
- Epigenetic Mechanisms Underlying Melanoma Resistance to Immune and Targeted Therapies.Cancers · 2022Review
- Stabilization of β-catenin promotes melanocyte specification at the expense of the Schwann cell lineage.Development (Cambridge, England) · 2022Article
- CDK7 and MITF repress a transcription program involved in survival and drug tolerance in melanoma.EMBO reports · 2021Article
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Melanoma cell phenotype switching between differentiated melanocytic and undifferentiated mesenchymal-like states drives metastasis and drug resistance. CDK7 is the serine/threonine kinase of the basal transcription factor TFIIH. We show that dedifferentiation of melanocytic-type melanoma cells into mesenchymal-like cells and acquisition of tolerance to targeted therapies is achieved through chronic inhibition of CDK7. In addition to emergence of a mesenchymal-type signature, we identify a GATA6-dependent gene expression program comprising genes such as AMIGO2 or ABCG2 involved in melanoma survival or targeted drug tolerance, respectively. Mechanistically, we show that CDK7 drives expression of the melanocyte lineage transcription factor MITF that in turn binds to an intronic region of GATA6 to repress its expression in melanocytic-type cells. We show that GATA6 expression is activated in MITF-low melanoma cells of patient-derived xenografts. Taken together, our data show how the poorly characterized repressive function of MITF in melanoma participates in a molecular cascade regulating activation of a transcriptional program involved in survival and drug resistance in melanoma.
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