ArticleOncogene2025
FRA1 drives melanoma metastasis through an actionable transcriptional network.
Article in Oncogene, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Allele-Specific GNAQ Q209 Mutations Reveal Context-Dependent Oncogenic Programs in Uveal Melanoma.Pigment cell & melanoma research · 2026Article
- A Multistep Immune-Competent Genetically Engineered Mouse Model Reveals Phenotypic Plasticity in Uveal Melanoma.Cancer research · 2026Article
- Transcriptional Reprogramming by AP-1-Bound Cis-Regulatory Elements Is Associated with Melanoma Development.International journal of molecular sciences · 2026Article
- Chromatin architecture and physical constriction cooperate in phenotype switching and cancer cell dissemination.bioRxiv : the preprint server for biology · 2026Article
- The SPA17-AXL axis drives melanoma aggressiveness and SPA17-targeting vaccination exhibits antitumor efficacy.Frontiers in immunology · 2026Article
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Authors and funding
11 authors.
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Abstract
Transcriptional dysregulation has emerged as a critical driver of melanoma progression, yet the molecular mechanisms governing this process and their potential as therapeutic targets remain inadequately characterized. Here, we identify FRA1 as a potent and actionable driver of melanoma metastasis. FRA1 enhanced both the initial seeding and subsequent outgrowth of metastatic lesions. Comprehensive multi-omics integration revealed transcriptional target genes of FRA1, with AXL, CDK6, and FSCN1 exhibiting increased expression in melanoma metastasis and a significant correlation with poor patient outcomes. Silencing AXL, CDK6, or FSCN1 abrogated FRA1-mediated invasion in vitro and reduced metastatic colonization. Furthermore, pharmacological inhibition of CDK6 and FSCN1, and to a lesser extent AXL, suppressed melanoma metastasis and prolonged overall survival. The expression of FRA1 and its target genes correlates with shortened survival across multiple cancer types, highlighting the broader clinical relevance of this pathway. This study unveils an actionable FRA1-mediated transcriptional network that drives cancer progression and metastasis, offering potential avenues for therapeutic interventions.
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