Overcoming EMT-driven therapeutic resistance by BH3 mimetics | Zendy

Ulrike Keitel | Zendy; Christina Scheel | Zendy; Matthias Dobbelstein | Zendy

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Overcoming EMT-driven therapeutic resistance by BH3 mimetics

Author(s) -

Ulrike Keitel,

Christina Scheel,

Matthias Dobbelstein

Publication year - 2014

Publication title -

oncoscience

Language(s) - English

Resource type - Journals

ISSN - 2331-4737

DOI - 10.18632/oncoscience.93

Subject(s) - epithelial–mesenchymal transition , cancer research , cancer , stroma , cancer cell , mechanism (biology) , cancer stem cell , apoptosis , biology , immunology , metastasis , genetics , philosophy , immunohistochemistry , epistemology

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.

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