ArticleEpigenetics2014
Aberrant CpG methylation of the TFAP2A gene constitutes a mechanism for loss of TFAP2A expression in human metastatic melanoma.
Article in Epigenetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- HNRNPC promotes progression of non-small cell lung cancer by maintaining TFAP2A mRNA stability.Cancer cell international · 2025Article
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- Molecular Biological Research on the Pathogenic Mechanism of Retinoblastoma.Current issues in molecular biology · 2024Review
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- AberrantBiomedicines · 2023Article
- Crucial role of the transcription factors family activator protein 2 in cancer: current clue and views.Journal of translational medicine · 2023Review
- Article
- The regulatory role of AP-2β in monoaminergic neurotransmitter systems: insights on its signalling pathway, linked disorders and theragnostic potential.Cell & bioscience · 2022Review
- EWSR1-ATF1 dependent 3D connectivity regulates oncogenic and differentiation programs in Clear Cell Sarcoma.Nature communications · 2022Article
- SWI/SNF Chromatin Remodeling Enzymes in Melanoma.Epigenomes · 2022Review
- Cooperation between melanoma cell states promotes metastasis through heterotypic cluster formation.Developmental cell · 2021Article
- Functional genomics of AP-2α and AP-2γ in cancers: in silico study.BMC medical genomics · 2020Article
- Bromodomain and extra-terminal domain (BET) proteins regulate melanocyte differentiation.Epigenetics & chromatin · 2020Article
- The biological characteristics of transcription factors AP-2α and AP-2γ and their importance in various types of cancers.Bioscience reports · 2019Review
- KIT Suppresses BRAFCancer research · 2017Article
- Beyond MITF: Multiple transcription factors directly regulate the cellular phenotype in melanocytes and melanoma.Pigment cell & melanoma research · 2017Review
- Association between Promoter Methylation of Gene ERCC3 and Benzene Hematotoxicity.International journal of environmental research and public health · 2017Article
- TFAP2 paralogs regulate melanocyte differentiation in parallel with MITF.PLoS genetics · 2017Article
- Article
- The Transcriptional Network Structure of a Myeloid Cell: A Computational Approach.International journal of genomics · 2017Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Metastatic melanoma is a deadly treatment-resistant form of skin cancer whose global incidence is on the rise. During melanocyte transformation and melanoma progression the expression profile of many genes changes. Among these, a gene implicated in several steps of melanocyte development, TFAP2A, is frequently silenced; however, the molecular mechanism of TFAP2A silencing in human melanoma remains unknown. In this study, we measured TFAP2A mRNA expression in primary human melanocytes compared to 11 human melanoma samples by quantitative real-time RT-PCR. In addition, we assessed CpG DNA methylation of the TFAP2A promoter in these samples using bisulfite sequencing. Compared to primary melanocytes, which showed high TFAP2A mRNA expression and no promoter methylation, human melanoma samples showed decreased TFAP2A mRNA expression and increased promoter methylation. We further show that increased CpG methylation correlates with decreased TFAP2A mRNA expression. Using The Cancer Genome Atlas, we further identified TFAP2A as a gene displaying among the most decreased expression in stage 4 melanomas vs. non-stage 4 melanomas, and whose CpG methylation was frequently associated with lack of mRNA expression. Based on our data, we conclude that TFAP2A expression in human melanomas can be silenced by aberrant CpG methylation of the TFAP2A promoter. We have identified aberrant CpG DNA methylation as an epigenetic mark associated with TFAP2A silencing in human melanoma that could have significant implications for the therapy of human melanoma using epigenetic modifying drugs.
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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.