Signaling Crosstalks: EGFR and TAZ in Breast Cancer
Breast cancer is driven by multiple molecular aberrations, transforming benign epithelial cells into metastatic cancer. Identification of key signaling nodes underlying metastasis and resistance to treatment is crucial to improving targeted therapies. This review examines two oncogenes driving ep...
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| Language: | en_US |
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The University of Arizona.
2017
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| Online Access: | http://hdl.handle.net/10150/625241 http://arizona.openrepository.com/arizona/handle/10150/625241 |
| Summary: | Breast cancer is driven by multiple molecular aberrations, transforming benign
epithelial cells into metastatic cancer. Identification of key signaling nodes underlying
metastasis and resistance to treatment is crucial to improving targeted therapies. This
review examines two oncogenes driving epithelial to mesenchymal transition (EMT) and
the acquisition of cancer stem cell properties. The epidermal growth factor receptor
(EGFR), a well-established oncogene driving migration, survival, and proliferation,
activates several downstream signaling cascades including the AKT and MAPK
pathways. EGFR overexpression, mutation, and mislocalization are frequently observed
in breast cancer. TAZ, transcriptional coactivator with PDZ-binding motif, induces and
sustains EMT and is required for the acquisition of breast cancer stem cell traits. The
emerging crosstalk between these pathways yields insights into early mammary
tumorigenesis, epithelial plasticity, and the metastatic niche, suggesting novel avenues
for the development of targeted therapies. |
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