ArticleEMBO molecular medicine2013
The neural crest transcription factor Brn3a is expressed in melanoma and required for cell cycle progression and survival.
Article in EMBO molecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Research Advances in Drug Resistance Mechanisms to Anti-HER2 Therapy in HER2-Positive Breast Cancer.Oncology research · 2026Review
- Identification of POU4F1 as a novel prognostic biomarker and therapeutic target in esophageal squamous cell carcinoma.Cancer cell international · 2024Article
- Activation of Bivalent Gene POU4F1 Promotes and Maintains Basal-like Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Immune escape and metastasis mechanisms in melanoma: breaking down the dichotomy.Frontiers in immunology · 2024Review
- HDAC2 Is Involved in the Regulation of BRN3A in Melanocytes and Melanoma.International journal of molecular sciences · 2022Article
- TGF-β Signaling: From Tissue Fibrosis to Tumor Microenvironment.International journal of molecular sciences · 2021Review
- Functional in vivo characterization of sox10 enhancers in neural crest and melanoma development.Communications biology · 2021Article
- Bone Morphogenic Protein Signaling and Melanoma.Current treatment options in oncology · 2021Review
- Transcriptome Analysis Reveals Differential Gene Expression between the Closing Ductus Arteriosus and the Patent Ductus Arteriosus in Humans.Journal of cardiovascular development and disease · 2021Article
- Immune Checkpoint Blockade in Advanced Cutaneous Squamous Cell Carcinoma: What Do We Currently Know in 2020?International journal of molecular sciences · 2020Review
- Loss of prdm1a accelerates melanoma onset and progression.Molecular carcinogenesis · 2020Article
- Neural transcription factor Pou4f1 promotes renal fibrosis via macrophage-myofibroblast transition.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- POU4F1 promotes the resistance of melanoma to BRAF inhibitors through MEK/ERK pathway activation and MITF up-regulation.Cell death & disease · 2020Article
- Transcription factors Brn-3α and TRIM16 in cancers, association with hormone reception.Heliyon · 2019Review
- Gene expression profiling informs HPV cervical histopathology but not recurrence/relapse after LEEP in ART-suppressed HIV+HPV+ women.Carcinogenesis · 2019Article
- Stem Cell-Derived Models of Neural Crest Are Essential to Understand Melanoma Progression and Therapy Resistance.Frontiers in molecular neuroscience · 2019Review
- Targeted Therapy-Resistant Melanoma Cells Acquire Transcriptomic Similarities with Human Melanoblasts.Cancers · 2018Article
- Ligand-activated BMP signaling inhibits cell differentiation and death to promote melanoma.The Journal of clinical investigation · 2018Article
- Pathways of aging: comparative analysis of gene signatures in replicative senescence and stress induced premature senescence.BMC genomics · 2016Article
- The lncRNA SLNCR1 Mediates Melanoma Invasion through a Conserved SRA1-like Region.Cell reports · 2016Article
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pigment cells and neuronal cells both are derived from the neural crest. Here, we describe the Pit-Oct-Unc (POU) domain transcription factor Brn3a, normally involved in neuronal development, to be frequently expressed in melanoma, but not in melanocytes and nevi. RNAi-mediated silencing of Brn3a strongly reduced the viability of melanoma cell lines and decreased tumour growth in vivo. In melanoma cell lines, inhibition of Brn3a caused DNA double-strand breaks as evidenced by Mre11/Rad50-containing nuclear foci. Activated DNA damage signalling caused stabilization of the tumour suppressor p53, which resulted in cell cycle arrest and apoptosis. When Brn3a was ectopically expressed in primary melanocytes and fibroblasts, anchorage-independent growth was increased. In tumourigenic melanocytes and fibroblasts, Brn3a accelerated tumour growth in vivo. Furthermore, Brn3a cooperated with proliferation pathways such as oncogenic BRAF, by reducing oncogene-induced senescence in non-malignant melanocytes. Together, these results identify Brn3a as a new factor in melanoma that is essential for melanoma cell survival and that promotes melanocytic transformation and tumourigenesis.
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Registered trials
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