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melanoma, cyld, cell, article, tggrm, cells, google, scholar, tumor, expression, cas, angiogenesis, mice, lymph, lines, tissue, progression, formation, fig, model, nature, rna, role, grm, proliferation, migration, germany, cancer, malignant, human, metastasis, signaling, timp, data, loss, growth, cyldknockout, mouse, compared, gene, generated, revealed, mrna, analyses, lymphatic, function, analysis, onset, sequencing, primary,

Topics {✒️}

nature portfolio german research foundation privacy policy animal research thermo fisher scientific affymetrix service provider nature 424 nature advertising cell index = relative change social media wnt/β-catenin pathway8 reprints cell index japan full size image unpaired t-test calculated anja-katrin bosserhoff immune-related gene signature predicted protein–protein interactions protein-protein interaction networks quantitative rt-pcr analyses nuclear envelope nano-topography beta1-integrin signaling pathways anti-tumorigenic protein independent tgf-beta target genes quantitative real-time pcr cyld-deficient mice compared cyld-knockout mice exhibits spontaneous melanoma development cyld-knockout mice compared qrt-pcr analyses revealed multiple tumor-suppressive functions microrna-622-regulated therapeutic target paraffin-embedded tissue blocks β-actin rev 5′-taaaacgcagctcagtaacagtccg-3′ c57bl/6 cyld-knockout mice19 cyld-knockout cell lines cyld-wildtype mice indicating cyld-deficiency promotes expression melanocyte-specific dct promoter permissions cyld-deficient melanoma tissue rna sequencing data tgf-beta signaling cyld-wildtype cell lines cyld-deficiency enhances proliferation providing c57bl/6 cyld−/−mice increasing incidence rates cyld-knockdown tissue compared

Questions {❓}

• Tg(Grm1) transgenic mice: a murine model that mimics spontaneous uveal melanoma in humans?

Schema {🗺️}

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         headline:Loss of CYLD accelerates melanoma development and progression in the Tg(Grm1) melanoma mouse model
         description:The deubiquitinase cylindromatosis (CYLD) is a well-known tumor suppressor, found to be down regulated in many cancer types including breast cancer, colon carcinoma and malignant melanoma. CYLD is suppressed in human melanoma cells by the transcriptional repressor SNAIL1 leading to an increase of their proliferative, invasive and migratory potential. To gain additional insights into the distinct function of this tumor suppressor gene a new mouse model Tg(Grm1)Cyld−/− was generated. Herewith, we demonstrate that Cyld-deficiency leads to earlier melanoma onset and accelerated tumor growth and metastasis in the GRM1 melanoma mouse model. First, RNA sequencing data revealed a potential role of CYLD in the regulation of genes involved in proliferation, migration and angiogenesis. Experiments using cell lines generated from both primary and metastatic melanoma tissue of Tg(Grm1) Cyld−/− and Tg(Grm1) Cyld+/+ mice confirmed that loss of CYLD enhances the proliferative and migratory potential, as well as the clonogenicity in vitro. Moreover, we could show that Cyld-knockout leads to increased vasculogenic mimicry and enhanced (lymph-) angiogenesis shown by tube formation assays, immunohistochemistry and mRNA expression analyses. In summary, our findings reveal new functional aspects of CYLD in the process of (lymph-) angiogenesis and demonstrate its importance in the early process of melanoma progression.
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      headline:Loss of CYLD accelerates melanoma development and progression in the Tg(Grm1) melanoma mouse model
      description:The deubiquitinase cylindromatosis (CYLD) is a well-known tumor suppressor, found to be down regulated in many cancer types including breast cancer, colon carcinoma and malignant melanoma. CYLD is suppressed in human melanoma cells by the transcriptional repressor SNAIL1 leading to an increase of their proliferative, invasive and migratory potential. To gain additional insights into the distinct function of this tumor suppressor gene a new mouse model Tg(Grm1)Cyld−/− was generated. Herewith, we demonstrate that Cyld-deficiency leads to earlier melanoma onset and accelerated tumor growth and metastasis in the GRM1 melanoma mouse model. First, RNA sequencing data revealed a potential role of CYLD in the regulation of genes involved in proliferation, migration and angiogenesis. Experiments using cell lines generated from both primary and metastatic melanoma tissue of Tg(Grm1) Cyld−/− and Tg(Grm1) Cyld+/+ mice confirmed that loss of CYLD enhances the proliferative and migratory potential, as well as the clonogenicity in vitro. Moreover, we could show that Cyld-knockout leads to increased vasculogenic mimicry and enhanced (lymph-) angiogenesis shown by tube formation assays, immunohistochemistry and mRNA expression analyses. In summary, our findings reveal new functional aspects of CYLD in the process of (lymph-) angiogenesis and demonstrate its importance in the early process of melanoma progression.
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         Apoptosis
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