ArticleOncogene2013
Mutant B-RAF regulates a Rac-dependent cadherin switch in melanoma.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
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- Acquired BRAFi Resistance Increases Melanoma Cell Sensitivity to Metabolic Targeting with Metformin.International journal of molecular sciences · 2026Article
- Review
- Skin Cancers and the Contribution of Rho GTPase Signaling Networks to Their Progression.Cancers · 2021Review
- Cellular Reprogramming-A Model for Melanoma Cellular Plasticity.International journal of molecular sciences · 2020Review
- ERK/MAPK Signaling Drives Overexpression of the Rac-GEF, PREX1, in BRAF- and NRAS-Mutant Melanoma.Molecular cancer research : MCR · 2016Article
- Article
- IRGM1 enhances B16 melanoma cell metastasis through PI3K-Rac1 mediated epithelial mesenchymal transition.Scientific reports · 2015Article
- SPARC Controls Melanoma Cell Plasticity through Rac1.PloS one · 2015Article
- ROBO1, a tumor suppressor and critical molecular barrier for localized tumor cells to acquire invasive phenotype: study in African-American and Caucasian prostate cancer models.International journal of cancer · 2014Article
- Molecular pathology of cutaneous melanoma.Melanoma management · 2014Review
- Melanoma: clinical features and genomic insights.Cold Spring Harbor perspectives in medicine · 2014Review
- ROCK inhibition activates MCF-7 cells.PloS one · 2014Article
- The role of the hippo pathway in melanocytes and melanoma.Frontiers in oncology · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The ability of cells to invade into the dermis is a critical event in the development of cutaneous melanoma and ultimately an indicator of poor prognosis. However, the molecular events surrounding the acquisition of this invasive phenotype remain incompletely understood. Mutations in B-RAF are frequent in melanoma and are known to regulate the invasive phenotype. In this study, we sought to determine the molecular mechanisms controlling melanoma invasion. We found that mutant B-RAF signaling regulates a cadherin switch. In melanoma cells expressing mutant B-RAF we observed high levels of N-cadherin and low levels of E-cadherin. Depletion of mutant B-RAF, by small interfering RNA, caused a decrease in the levels of N-cadherin and an increase in the levels of E-cadherin. Mechanistically, we found that this cadherin switch required the activity of Rac1 and its GEF, Tiam1, both of which show suppressed activity in the presence of mutant B-RAF. Consistent with the work of others, we found that depletion of mutant B-RAF decreased the invasive capacity of the melanoma cells. However, simultaneous depletion of B-RAF and Rac or Tiam1 resulted in invasive capacity similar to that of control cells. Taken together, our results suggest that mutant B-RAF signaling downregulates Tiam1/Rac activity resulting in an increase in N-cadherin levels and a decrease in E-cadherin levels and ultimately enhanced invasion.
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Registered trials
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