ArticleOncogene2008
Oncogene activation in melanocytes links reactive oxygen to multinucleated phenotype and senescence.
Article in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 85 citations in OpenAlex.
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- FGF-2 induces a failure of cell cycle progression in cells harboring amplified K-Ras, revealing new insights into oncogene-induced senescence.Molecular omics · 2021Article
- The combination of mitogenic stimulation and DNA damage induces chondrocyte senescence.Osteoarthritis and cartilage · 2021Article
- The transcription factor NRF2 enhances melanoma malignancy by blocking differentiation and inducing COX2 expression.Oncogene · 2020Article
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- DNA replication stress: oncogenes in the spotlight.Genetics and molecular biology · 2019Article
- Multi-nucleated cells use ROS to induce breast cancer chemo-resistance in vitro and in vivo.Oncogene · 2018Article
- Mechanisms of Oncogene-Induced Replication Stress: Jigsaw Falling into Place.Cancer discovery · 2018Review
- A common intronic variant of PARP1 confers melanoma risk and mediates melanocyte growth via regulation of MITF.Nature genetics · 2017Article
- Glucose availability controls ATF4-mediated MITF suppression to drive melanoma cell growth.Oncotarget · 2017Article
- Article
- The Long Noncoding RNA SPRIGHTLY Regulates Cell Proliferation in Primary Human Melanocytes.The Journal of investigative dermatology · 2016Article
- Reactivation of p53 by a Cytoskeletal Sensor to Control the Balance Between DNA Damage and Tumor Dissemination.Journal of the National Cancer Institute · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Contrary to malignant melanoma, nevi are a benign form of melanocytic hyperproliferation. They are frequently observed as precursor lesions of melanoma, but they also feature biochemical markers of senescence. In particular, evidence for oncogene-induced melanocyte senescence as natural means to prevent tumorigenesis has been obtained in nevi with mutated B-Raf(V600E). Here, we demonstrate that strong oncogenic growth factor receptor signalling drives melanocytes into senescence, whereas weaker signals keep them in the proliferative state. Activation of oncogene-induced senescence also produces multinucleated giant cells, a long known histological feature of nevus cells. The protein levels of the senescence mediators, p53 and pRB, and their upstream activators do not correlate with senescence. However, strong oncogene signalling leads to pronounced reactive oxygen stress, and scavenging of reactive oxygen species (ROS) efficiently prevents the formation of multinucleated cells and senescence. Similarly, expression of oncogenic N-RAS results in ROS generation, DNA damage and the same multinuclear senescent phenotype. Hence, we identified oncogenic signalling-dependent ROS production as critical mediator of the melanocytic multinuclear phenotype and senescence, both of them being hallmarks of human nevus cells.
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