title: Overcoming EMT-driven therapeutic resistance by BH3 mimetics.
abstract: Epithelial-mesenchymal transition (EMT) contributes to the progression of cancer through enhanced invasion and stem-like properties of cancer cells. Additionally, EMT confers resistance towards many chemotherapeutics. We recently described a mechanism that mediates EMT-driven chemoresistance through augmented levels of Bcl-xL, an anti-apoptotic member of the Bcl-2 family (Keitel et al., Oncotarget, in press). Here, we elaborate on how these findings pertain to cancer cells dispersed in the tumor-adjacent stroma of breast cancer tissues, and how BH3-mimetics may provide a therapeutic strategy to eliminate cancer cell populations that have passed through an EMT.
authors.affiliation: Institute of Molecular Oncology, Göttingen Center of Molecular Biosciences (GZMB), Faculty of Medicine, University of Göttingen, Göttingen, Germany.
authors.forename: Ulrike
authors.initials: U
authors.lastname: Keitel
authors.affiliation: Institute for Stem Cell Research, Helmholtz Center Munich, Neuherberg, Germany.
authors.forename: Christina
authors.initials: C
authors.lastname: Scheel
authors.affiliation: Institute of Molecular Oncology, Göttingen Center of Molecular Biosciences (GZMB), Faculty of Medicine, University of Göttingen, Göttingen, Germany.
authors.forename: Matthias
authors.initials: M
authors.lastname: Dobbelstein
keywords: EMT; HMEC; HMLE