Abstract
Abstract Introduction Invasion and metastasis are the main causes for the death of patients with breast cancers. Epithelial–mesenchy-mal transition is implicated as a vital process in the invasion and metasta -sis of breast cancers, with endowing migratory and invasive cancer cells associated with metastatic capabil-ity. Increasing evidences demon -strated that epithelial–mesenchymal tions. However, this process is retransition-initiating cells possessed mesenchymal features and stem-like traits that are resistant to chemother-apy. In this review, we summarise the physiological and pathological roles of epithelial–mesenchymal transi-tions, new insights in the molecular mechanisms of regulating epithe-lial–mesenchymal transition during breast cancer invasion and metasta -sis, and its implication in chemother-apy resistance. Conclusion Therefore, it is challenging to probe and uncover the mechanistic regu -lation of oncogenic epithelial–mes-enchymal transition, which will contribute to our understanding of metastatic dissemination and the role of targeting epithelial–mesenchymal transition with existing therapy as well as developing new drugs, in order to prevent metastasis and to diminish distant recurrence in pa -tients with breast cancers.
Highlights
Invasion and metastasis are the main causes for the death of patients with breast cancers
Epithelial–mesenchymal transition (EMT), which is known as the probable first step in the complex process of metastasis, is a distinctive morphological change, in which the series of events converting the epithelial cancer cells switch from a well-differentiated, adherent phenotype to an individual, invasive migratory mesenchymal cell[2]
EMT is supposed to be associated with cancer stem cells (CSCs), by generating self-renewing cells, which is contributed to the tumorigenesis and multi-drug resistance4.
Summary
Invasion and metastasis are the main causes for the death of patients with breast cancers. Epithelial–mesenchymal transition is implicated as a vital process in the invasion and metastasis of breast cancers, with endowing migratory and invasive cancer cells associated with metastatic capability. Increasing evidences demonstrated that epithelial–mesenchymal transition-initiating cells possessed mesenchymal features and stem-like traits that are resistant to chemotherapy. We summarise the physiological and pathological roles of epithelial–mesenchymal transitions, new insights in the molecular mechanisms of regulating epithelial–mesenchymal transition during breast cancer invasion and metastasis, and its implication in chemotherapy resistance. Epithelial–mesenchymal transition (EMT), which is known as the probable first step in the complex process of metastasis, is a distinctive morphological change, in which the series of events converting the epithelial cancer cells switch from a well-differentiated, adherent phenotype to an individual, invasive migratory mesenchymal cell[2]. EMT is supposed to be associated with cancer stem cells (CSCs), by generating self-renewing cells, which is contributed to the tumorigenesis and multi-drug resistance4.
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