Epithelial-mesenchymal transition in breast cancer progression and metastasis

Abstract

Breast cancer is the most common cancer in women, and approximately 90% of breast cancer deaths are caused by local invasion and distant metastasis of tumor cells. Epithelial-mesenchymal transition (EMT) is a vital process for large-scale cell movement during morphogenesis at the time of embryonic development. Tumor cells usurp this developmental program in order to execute the multi-step process of tumorigenesis and metastasis. Several transcription factors and signals are involved in these events. In this review, we summarize some recent advances in breast cancer research that have provided new insights in the molecular mechanisms underlying the regulation of EMT during breast cancer progression and metastasis. We especially focus on the molecular pathways that control EMT.

Claudin-4 SPECT Imaging Allows Detection of Aplastic Lesions in a Mouse Model of Breast Cancer

“…Claudins in general and claudin-4 in particular have a known involvement in epithelial-to-mesenchymal transition (EMT), the complex stepwise phenomenon that occurs during both embryonic development and very-early during tumorigenesis (25). A recent link between EMT and cancer stem cells has sparked considerable interest, because it is widely accepted that only a minor population of tumor cells can initiate and support the development of tumors, and the highly aggressive tumor cells share many characteristics of embryonic progenitor cells.…”

Development of nanotheranostics against metastatic breast cancer — A focus on the biology & mechanistic approaches

“…These complex sets of events disrupt mainly the tight junctions, desmosomes and promote the transition of epithelial to transient mesenchymal cells via type 3 EMT (Foroni et al, 2012). Motility, invasiveness, and anokis resistance of the metastatic breast cancer cells are derived from oncogenic epithelial to mesenchymal transition (EMT) through the loss of E-cadherin expression with the increase in fibroid morphology (Drasin et al, 2011;Wang and Zhou, 2011;Dave et al, 2012). Cells undergoing EMT, attack the adjacent stroma resulting in the invasion and intravasation of cells in the circulation either individually or as mass.…”

Suppression of the Epidermal Growth Factor Receptor Inhibits Epithelial–Mesenchymal Transition in Human Pancreatic Cancer PANC-1 Cells

“…An important molecular event is the overexpression of epidermal growth factor receptor (EGFR) and activation of its downstream signaling [4]. Two recent studies have indicated that EGFR was detectable in more than 95% of patients with pancreatic cancer [5,6].…”