Epithelial-mesenchymal transition in breast cancer

One of the key molecular mechanisms contributing to the metastatic progression is epithelial to mesenchymal transition (EMT), which drives invasion and migration of various cancer including breast cancer.During tumorigenesis, changes in EMT regulatory pathways lead to a loss of cellular adhesions, changes in the polarization of the cell and cytoskeleton, detachment, migration, intra-vasation, and survival in the vascular system; extravasation, and finally, metastasis.EMT is largely mediated by a core set of EMT-activating transcription factors. The master regulators of the EMT include many pathways, however the primary mediators of the EMT include signaling through TGF-, Notch and Wnt.  The role of EMT in breast cancer has  been demonstrated via numerous in vitro studies in  normal and malignant mammary epithelial cells and via in vivo studies using mouse models of breast cancers. Studying the regulatory pathways of the EMT process can be used as a tool for cancer monitoring ,treatment and possible direct targets for new-combination anticancer personalized medicine.

کلیدواژه ها:

Epithelial to mesenchymal transition ، Breast cancer ، Cell Signaling ، Personalized Medicine