ArticleMolecular therapy oncolytics2020
Mithramycin A and Mithralog EC-8042 Inhibit SETDB1 Expression and Its Oncogenic Activity in Malignant Melanoma.
Article in Molecular therapy oncolytics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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The trial behind it
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Who cites it
24 citing papers in PubMed, 48 citations in OpenAlex.
- SETDB1 promotes gastric cancer progression via UPR and mTOR pathway.Cancer cell international · 2026Article
- Myricetin Inhibits Osteosarcoma Cell Viability and Modulates EMT-Related Genes Associated with thePharmaceuticals (Basel, Switzerland) · 2026Article
- The Role of Histone Methyltransferase SETDB1 in Normal and Malignant Hematopoiesis.Cancer science · 2025Review
- Cancer cell type-specific derepression of transposable elements by inhibition of chromatin modifier enzymes.Communications biology · 2025Article
- Identification and clinical implications of endogenous retrovirus elements suppressed by SETDB1 in hepatocellular carcinoma.JHEP reports : innovation in hepatology · 2025Article
- Targeting SETDB1 in cancer and immune regulation: Potential therapeutic strategies in cancer.The Kaohsiung journal of medical sciences · 2025Review
- Article
- SETDB1: an emerging target for anticancer drug development.Future medicinal chemistry · 2025Article
- Integrative analysis of transcriptome, DNA methylome, and chromatin accessibility reveals candidate therapeutic targets in hypertrophic cardiomyopathy.Protein & cell · 2024Article
- SETDB1 as a cancer target: challenges and perspectives in drug design.RSC medicinal chemistry · 2024Review
- Targeting SMAD-Dependent Signaling: Considerations in Epithelial and Mesenchymal Solid Tumors.Pharmaceuticals (Basel, Switzerland) · 2024Review
- The function of histone methyltransferase SETDB1 and its roles in liver cancer.Frontiers in cell and developmental biology · 2024Review
- The functions of SET domain bifurcated histone lysine methyltransferase 1 (SETDB1) in biological process and disease.Epigenetics & chromatin · 2023Review
- Secretogranin II influences the assembly and function of MHC class I in melanoma.Experimental hematology & oncology · 2023Article
- Review
- Epigenetic Mechanisms Underlying Melanoma Resistance to Immune and Targeted Therapies.Cancers · 2022Review
- "Stripe" transcription factors provide accessibility to co-binding partners in mammalian genomes.Molecular cell · 2022Article
- Differential Impact of Random GC Tetrad Binding and Chromatin Events on Transcriptional Inhibition by Olivomycin A.International journal of molecular sciences · 2022Article
- SETDB1 acts as a topological accessory to Cohesin via an H3K9me3-independent, genomic shunt for regulating cell fates.Nucleic acids research · 2022Article
- Mechanisms of Immunotherapy Resistance in Cutaneous Melanoma: Recognizing a Shapeshifter.Frontiers in oncology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Malignant melanoma is the most deadly skin cancer, associated with rising incidence and mortality rates. Most of the patients with melanoma, treated with current targeted therapies, develop a drug resistance, causing tumor relapse. The attainment of a better understanding of novel cancer-promoting molecular mechanisms driving melanoma progression is essential for the development of more effective targeted therapeutic approaches. Recent studies, including the research previously conducted in our laboratory, reported that the histone methyltransferase SETDB1 contributes to melanoma pathogenesis. In this follow-up study, we further elucidated the role of SETDB1 in melanoma, showing that SETDB1 modulated relevant transcriptomic effects in melanoma, in particular, as activator of cancer-related secreted (CRS) factors and as repressor of melanocyte-lineage differentiation (MLD) and metabolic enzymes. Next, we investigated the effects of SETDB1 inhibition via compounds belonging to the mithramycin family, mithramycin A and mithramycin analog (mithralog) EC-8042: melanoma cells showed strong sensitivity to these drugs, which effectively suppressed the expression of SETDB1 and induced changes at the transcriptomic, morphological, and functional level. Moreover, SETDB1 inhibitors enhanced the efficacy of mitogen-activated protein kinase (MAPK) inhibitor-based therapies against melanoma. Taken together, this work highlights the key regulatory role of SETDB1 in melanoma and supports the development of SETDB1-targeting therapeutic strategies for the treatment of melanoma patients.
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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.