An Abl target in metastatic melanoma
Melanoma cells secrete proteases called cathepsins, which degrade the extracellular matrix and facilitate cell migration and invasion. Tripathi et al. found that cathepsin secretion was promoted by the nonreceptor tyrosine kinase Abl. Activation of Abl or a related kinase Arg promoted cathepsin B and cathepsin L expression and secretion by cell type–specific mechanisms involving transcription factors associated with the epithelial-mesenchymal transition and cancer progression. Analysis in a mouse model of metastatic melanoma suggested that Abl and Arg inhibitors may be a way to inhibit cathepsins and treat patients with metastatic melanoma.
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