ArticleThe EMBO journal1998
Loss of AP-2 results in downregulation of c-KIT and enhancement of melanoma tumorigenicity and metastasis.
Article in The EMBO journal, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 257 citations in OpenAlex.
- Transcription factor activating enhancer-binding protein 2ε (AP2ε) modulates phenotypic plasticity and progression of malignant melanoma.Cell death & disease · 2024Article
- Epigenetically modified AP-2α by DNA methyltransferase facilitates glioma immune evasion by upregulating PD-L1 expression.Cell death & disease · 2023Article
- PCDH1 promotes progression of pancreatic ductal adenocarcinoma via activation of NF-κB signalling by interacting with KPNB1.Cell death & disease · 2022Article
- TFAP2 paralogs facilitate chromatin access for MITF at pigmentation and cell proliferation genes.PLoS genetics · 2022Article
- A novel anti-c-Kit antibody-drug conjugate to treat wild-type and activating-mutant c-Kit-positive tumors.Molecular oncology · 2022Article
- The mucin protein MUCL1 regulates melanogenesis and melanoma genes in a manner dependent on threonine content.The British journal of dermatology · 2022Article
- Cooperation between melanoma cell states promotes metastasis through heterotypic cluster formation.Developmental cell · 2021Article
- AP-2α-Mediated Activation of E2F and EZH2 Drives Melanoma Metastasis.Cancer research · 2021Article
- Cyclic adenosine monophosphate (cAMP) signaling in melanocyte pigmentation and melanomagenesis.Pigment cell & melanoma research · 2021Review
- Upregulation of the transcription factor TFAP2D is associated with aggressive tumor phenotype in prostate cancer lacking the TMPRSS2:ERG fusion.Molecular medicine (Cambridge, Mass.) · 2020Article
- The miR-26a/AP-2α/Nanog signaling axis mediates stem cell self-renewal and temozolomide resistance in glioma.Theranostics · 2019Article
- KIT Suppresses BRAFCancer research · 2017Article
- Long Noncoding RNA BC032913 as a Novel Therapeutic Target for Colorectal Cancer that Suppresses Metastasis by Upregulating TIMP3.Molecular therapy. Nucleic acids · 2017Article
- Beyond MITF: Multiple transcription factors directly regulate the cellular phenotype in melanocytes and melanoma.Pigment cell & melanoma research · 2017Review
- miR-10a suppresses colorectal cancer metastasis by modulating the epithelial-to-mesenchymal transition and anoikis.Cell death & disease · 2017Article
- TFAP2 paralogs regulate melanocyte differentiation in parallel with MITF.PLoS genetics · 2017Article
- Article
- DAB2IP regulates cancer stem cell phenotypes through modulating stem cell factor receptor and ZEB1.Oncogene · 2015Article
- microRNA-217 inhibits tumor progression and metastasis by downregulating EZH2 and predicts favorable prognosis in gastric cancer.Oncotarget · 2015Article
- Article
18 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Expression of the tyrosine kinase receptor, c-KIT, progressively decreases during local tumor growth and invasion of human melanomas. We have previously shown that enforced c-KIT expression in highly metastatic cells inhibited tumor growth and metastasis in nude mice. Furthermore, the ligand for c-KIT, SCF, induces apoptosis in human melanoma cells expressing c-KIT under both in vitro and in vivo conditions. Here we show that loss of c-KIT expression in highly metastatic cells correlates with loss of expression of the transcription factor AP-2. The c-KIT promoter contains three binding sites for AP-2 and EMSA gels demonstrated that AP-2 protein binds directly to the c-KIT promoter. Transfection of wild-type AP-2 into c-KIT-negative A375SM melanoma cells activated a c-KIT promoter-driven luciferase reporter gene, while expression of a dominant-negative AP-2B in c-KIT-positive Mel-501 cells inhibited its activation. Endogenous c-KIT mRNA and expression of proteins were upregulated in AP-2-transfected cells, but not in control cells. In addition, re-expression of AP-2 in A375SM cells suppressed their tumorigenicity and metastatic potential in nude mice. These results indicate that the expression of c-KIT is highly regulated by AP-2 and that enforced AP-2 expression suppresses tumorigenicity and metastatic potential of human melanoma cells, possibly through c-KIT transactivation and SCF-induced apoptosis. Therefore, loss of AP-2 expression might be a crucial event in the development of malignant melanoma.
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