Control of MT1-MMP transport by atypical PKC during breast-cancer progression
Nom de la revue
Proceedings of the National Academy of Sciences
Abstract
Significance
We characterize a mechanism through which the polarity protein atypical PKCι controls invasion and matrix remodeling by tumor cells by regulating endosome-to-plasma membrane traffic of the membrane type 1-matrix metalloproteinase (MT1-MMP) in breast-cancer cells. Further analysis shows that atypical PKCι and MT1-MMP are co–up-regulated in hormone receptor-negative breast tumors in association with higher risk of metastasis. These findings provide previously unidentified avenues for the design of therapeutic interventions.