ArticleMolecular biology of the cell2021
Uveal melanoma cells use ameboid and mesenchymal mechanisms of cell motility crossing the endothelium.
Article in Molecular biology of the cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Functions and clinical implications of the liver microenvironment in hepatic uveal melanoma metastases.Cancer metastasis reviews · 2025Review
- Guanine Nucleotide Exchange Factors and Small GTPases: Their Regulation and Functions, Diseases, and Therapeutic Targets.MedComm · 2025Review
- Presence of tumor DNA in aqueous humor is correlated with high risk uveal melanoma.Scientific reports · 2025Article
- New Insights into the Exosome-Induced Migration of Uveal Melanoma Cells and the Pre-Metastatic Niche Formation in the Liver.Cancers · 2024Article
- Uveal Melanoma: Comprehensive Review of Its Pathophysiology, Diagnosis, Treatment, and Future Perspectives.Biomedicines · 2024Review
- EHMT2 promotes tumorigenesis inActa pharmaceutica Sinica. B · 2024Article
- Prognostic Biomarkers in Uveal Melanoma: The Status Quo, Recent Advances and Future Directions.Cancers · 2021Review
- Uveal Melanoma Metastasis.Cancers · 2021Review
- Septin and actin contributions to endothelial cell-cell junctions and monolayer integrity.Cytoskeleton (Hoboken, N.J.)Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Uveal melanomas (UMs) are malignant cancers arising from the pigmented layers of the eye. UM cells spread through the bloodstream, and circulating UM cells are detectable in patients before metastases appear. Extravasation of UM cells is necessary for formation of metastases, and transendothelial migration (TEM) is a key step in extravasation. UM cells execute TEM via a stepwise process involving the actin-based processes of ameboid blebbing and mesenchymal lamellipodial protrusion. UM cancers are driven by oncogenic mutations that activate Gαq/11, and this activates TRIO, a guanine nucleotide exchange factor for RhoA and Rac1. We found that pharmacologic inhibition of Gαq/11 in UM cells reduced TEM. Inhibition of the RhoA pathway blocked amoeboid motility but led to enhanced TEM; in contrast, inhibition of the Rac1 pathway decreased mesenchymal motility and reduced TEM. Inhibition of Arp2/3 complex allowed cells to transmigrate without intercalation, a direct mechanism similar to the one often displayed by immune cells. BAP1-deficient (+/-) UM subclones displayed motility behavior and increased levels of TEM, similar to the effects of RhoA inhibitors. We conclude that RhoA and Rac1 signaling pathways, downstream of oncogenic Gαq/11, combine with pathways regulated by BAP1 to control the motility and transmigration of UM cells.
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