ArticleOncogene2017
The AP-1 transcription factor FOSL1 causes melanocyte reprogramming and transformation.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.
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Who cites it
65 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.
- Meta-analysis of microarray data to identify potential signature genes and MiRNAs associated with the pathogenesis of asthma.Journal of translational medicine · 2025Pooled it
- Mechanistic modeling reveals a configurable AP-1 network governing cell-state heterogeneity and adaptive plasticity in melanoma cells.Cell reports · 2026Article
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- BMP4 cocktail promotes utricular progenitor reprogramming and vestibular functional recovery in adult mice.Journal of advanced research · 2026Article
- Transcriptional Reprogramming by AP-1-Bound Cis-Regulatory Elements Is Associated with Melanoma Development.International journal of molecular sciences · 2026Article
- MITF Is an Essential and Functionally Multifaceted Transcription Factor in Cutaneous Melanoma.Cancers · 2026Review
- From paradox to target: IFN-β hijacks MEK signaling to drive a cell death-evading dormant phenotype in colorectal cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- FOSL1 promotes homologous recombination repair and camptothecin resistance via TCOF1-mediated ribosome biogenesis in non-small cell lung cancer.Translational oncology · 2026Article
- Integrated single-cell and spatial transcriptomic profiling decodes lineage plasticity and immune microenvironment remodeling in prostate cancer progression.Molecular cancer · 2026Article
- Inhibition of FOS-Like Antigen 1 Reduces Chemoresistance to Temozolomide Through Stemness Reprogramming via IL-6/STAT3MedComm · 2026Article
- The role of HMGA1 in genome stability: Implications in human cancer.Cellular and molecular life sciences : CMLS · 2026Review
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- Neutrophil extracellular traps-STC1 positive feedback loop promotes immune evasion and metastasis in bladder cancer.Journal for immunotherapy of cancer · 2025Article
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- A 14-bp motif in the KIT active promoter region is critical for melanin accumulation in yaks, mice, and humans.BMC biology · 2025Article
- Gene-expression signature predicts autoimmune toxicity in metastatic melanoma.Journal for immunotherapy of cancer · 2025Article
- FOSL1 promotes keratinocyte migration and wound repair by modulating the IL17 signaling pathway.Scientific reports · 2025Article
- Cooperation between the Hippo and MAPK pathway activation drives acquired resistance to TEAD inhibition.Nature communications · 2025Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The MAPK pathway is activated in the majority of melanomas and is the target of therapeutic approaches. Under normal conditions, it initiates the so-called immediate early response, which encompasses the transient transcription of several genes belonging to the AP-1 transcription factor family. Under pathological conditions, such as continuous MAPK pathway overactivation due to oncogenic alterations occurring in melanoma, these genes are constitutively expressed. The consequences of a permanent expression of these genes are largely unknown. Here, we show that FOSL1 is the main immediate early AP-1 member induced by melanoma oncogenes. We first examined its role in established melanoma cells. We found that FOSL1 is involved in melanoma cell migration as well as cell proliferation and anoikis-independent growth, which is mediated by the gene product of its target gene HMGA1, encoding a multipotent chromatin modifier. As FOSL1 expression is increased in patient melanoma samples compared to nevi, we investigated the effect of enhanced FOSL1 expression on melanocytes. Intriguingly, we found that FOSL1 acts oncogenic and transforms melanocytes, enabling subcutaneous tumor growth in vivo. During the process of transformation, FOSL1 reprogrammed the melanocytes and downregulated MITF in a HMGA1-dependent manner. At the same time, AXL was upregulated, leading to a shift in the MITF/AXL balance. Furthermore, FOSL1 re-enforced pro-tumorigenic transcription factors MYC, E2F3 and AP-1. Together, this led to the enhancement of several growth-promoting processes, such as ribosome biogenesis, cellular detachment and pyrimidine metabolism. Overall, we demonstrate that FOSL1 is a novel reprogramming factor for melanocytes with potent tumor transformation potential.
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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.