ArticleMolecular carcinogenesis2016
The Ezh2 polycomb group protein drives an aggressive phenotype in melanoma cancer stem cells and is a target of diet derived sulforaphane.
Article in Molecular carcinogenesis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 60 citations in OpenAlex.
- Natural modulators of enhancer of zeste homolog 2 (EZH2): potential epigenetic regulators of aging-associated pathways.Biogerontology · 2026Review
- Sulforaphane as a Multi-Scale Mechano-Modulator in Cancer: An Integrative Perspective.Biology · 2026Article
- EZH2 in Acral Lentiginous Melanoma: Molecular, Epigenetic, and Therapeutic Perspectives.Oncology research · 2026Review
- Molecular reprogramming in cutaneous melanoma: the central role of G9a and EZH2 methyltransferase inhibitors in tumor plasticity, immune evasion, and therapeutic resistance.Frontiers in pharmacology · 2026Review
- Potential mechanisms of cancer prevention and treatment by sulforaphane, a natural small molecule compound of plant-derived.Molecular medicine (Cambridge, Mass.) · 2024Review
- Anti-Inflammatory Therapeutic Mechanisms of Isothiocyanates: Insights from Sulforaphane.Biomedicines · 2024Review
- Resistance to BRAF Inhibitors: EZH2 and Its Downstream Targets as Potential Therapeutic Options in Melanoma.International journal of molecular sciences · 2023Article
- Study on pharmacokinetic interactions between SHR2554 and itraconazole in healthy subjects: A single-center, open-label phase I trial.Cancer medicine · 2023Article
- Combinatorial epigenetic mechanisms of sulforaphane, genistein and sodium butyrate in breast cancer inhibition.Experimental cell research · 2022Article
- Sulforaphane covalently interacts with the transglutaminase 2 cancer maintenance protein to alter its structure and suppress its activity.Molecular carcinogenesis · 2022Article
- Benzyl and phenethyl isothiocyanates as promising epigenetic drug compounds by modulating histone acetylation and methylation marks in malignant melanoma.Investigational new drugs · 2021Article
- Targeting Cancer Stem Cells by Dietary Agents: An Important Therapeutic Strategy against Human Malignancies.International journal of molecular sciences · 2021Review
- Review
- AP-2α-Mediated Activation of E2F and EZH2 Drives Melanoma Metastasis.Cancer research · 2021Article
- Sulforaphane inhibits PRMT5 and MEP50 function to suppress the mesothelioma cancer cell phenotype.Molecular carcinogenesis · 2021Article
- Predictive biomarkers and potential drug combinations of epi-drugs in cancer therapy.Clinical epigenetics · 2021Review
- Polycomb complexes redundantly maintain epidermal stem cell identity during development.Genes & development · 2021Article
- Allyl isothiocyanate regulates lysine acetylation and methylation marks in an experimental model of malignant melanoma.European journal of nutrition · 2020Article
- The YAP1 Signaling Inhibitors, Verteporfin and CA3, Suppress the Mesothelioma Cancer Stem Cell Phenotype.Molecular cancer research : MCR · 2020Article
- Epigenetic Silencing of CDR1as Drives IGF2BP3-Mediated Melanoma Invasion and Metastasis.Cancer cell · 2020Article
Corrections and comments
- Erratum issuedCorrigendum.2017
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Melanoma is a metastatic cancer associated with poor survival. Here, we study a subpopulation of melanoma cancer cells displaying melanoma cancer stem cell (MCS cells) properties including elevated expression of stem cell markers, increased ability to survive as spheroids, and enhanced cell migration and invasion. We show that the Ezh2 stem cell survival protein is enriched in MCS cells and that Ezh2 knockdown or treatment with small molecule Ezh2 inhibitors, GSK126 or EPZ-6438, reduces Ezh2 activity. This reduction is associated with a reduced MCS cell spheroid formation, migration, and invasion. Moreover, the diet-derived cancer prevention agent, sulforaphane (SFN), suppresses MCS cell survival and this is associated with loss of Ezh2. Forced expression of Ezh2 partially reverses SFN suppression of MCS cell spheroid formation, migration, and invasion. A375 melanoma cell-derived MCS cells form rapidly growing tumors in immune-compromised mice and SFN treatment of these tumors reduces tumor growth and this is associated with reduced Ezh2 level and H3K27me3 formation, reduced matrix metalloproteinase expression, increased TIMP3 expression and increased apoptosis. These studies identify Ezh2 as a MCS cell marker and cancer stem cell prevention target, and suggest that SFN acts to reduce melanoma tumor formation via a mechanism that includes suppression of Ezh2 function. © 2015 Wiley Periodicals, Inc.
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