ArticlePLoS biology2013
The Rho exchange factors Vav2 and Vav3 favor skin tumor initiation and promotion by engaging extracellular signaling loops.
Article in PLoS biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 71 citations in OpenAlex.
- RAC1 signaling in prostate cancer: VAV GEFs take center stage.Frontiers in cell and developmental biology · 2025Article
- Pan-cancer analyses identify oncogenic drivers, expression signatures, and therapeutic vulnerabilities in RHO GTPase pathway genes.Frontiers in bioinformatics · 2025Article
- Neryl acetate, the major component of Corsican Helichrysum italicum essential oil, mediates its biological activities on skin barrier.PloS one · 2023Article
- Article
- The Rho GTPase exchange factor Vav2 promotes extensive age-dependent rewiring of the hair follicle stem cell transcriptome.Frontiers in cell and developmental biology · 2023Article
- Loss of Amphiregulin drives inflammation and endothelial apoptosis in pulmonary hypertension.Life science alliance · 2022Article
- Characterization of the spectrum of trivalent VAV1-mutation-driven tumours using a gene-edited mouse model.Molecular oncology · 2022Article
- The Rho guanosine nucleotide exchange factors Vav2 and Vav3 modulate epidermal stem cell function.Oncogene · 2022Article
- Nuclear Vav3 is required for polycomb repression complex-1 activity in B-cell lymphoblastic leukemogenesis.Nature communications · 2022Article
- Cancer-associated mutations in VAV1 trigger variegated signaling outputs and T-cell lymphomagenesis.The EMBO journal · 2021Article
- RHO GTPase-Related Long Noncoding RNAs in Human Cancers.Cancers · 2021Review
- Review
- New Functions of Vav Family Proteins in Cardiovascular Biology, Skeletal Muscle, and the Nervous System.Biology · 2021Review
- Skin Cancers and the Contribution of Rho GTPase Signaling Networks to Their Progression.Cancers · 2021Review
- Article
- VAV2 signaling promotes regenerative proliferation in both cutaneous and head and neck squamous cell carcinoma.Nature communications · 2020Article
- Article
- Rho guanosine nucleotide exchange factors are not such bad guys after all in cancerSmall GTPases · 2020Article
- Vav2 pharmaco-mimetic mice reveal the therapeutic value and caveats of the catalytic inactivation of a Rho exchange factor.Oncogene · 2020Article
- High-Throughput Sequencing Identifies 3 Novel Susceptibility Genes for Hereditary Melanoma.Genes · 2020Article
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The catalytic activity of GDP/GTP exchange factors (GEFs) is considered critical to maintain the typically high activity of Rho GTPases found in cancer cells. However, the large number of them has made it difficult to pinpoint those playing proactive, nonredundant roles in tumors. In this work, we have investigated whether GEFs of the Vav subfamily exert such specific roles in skin cancer. Using genetically engineered mice, we show here that Vav2 and Vav3 favor cooperatively the initiation and promotion phases of skin tumors. Transcriptomal profiling and signaling experiments indicate such function is linked to the engagement of, and subsequent participation in, keratinocyte-based autocrine/paracrine programs that promote epidermal proliferation and recruitment of pro-inflammatory cells. This is a pathology-restricted mechanism because the loss of Vav proteins does not cause alterations in epidermal homeostasis. These results reveal a previously unknown Rho GEF-dependent pro-tumorigenic mechanism that influences the biology of cancer cells and their microenvironment. They also suggest that anti-Vav therapies may be of potential interest in skin tumor prevention and/or treatment.
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Registered trials
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.