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Epithelial–mesenchymal transition was first recognized as a feature of embryogenesis by Betty Hay in the 1980s. [ 1 ] [ 2 ] EMT, and its reverse process, MET ( mesenchymal-epithelial transition ) are critical for development of many tissues and organs in the developing embryo, and numerous embryonic events such as gastrulation , neural crest ...
The epithelial-menenchymal transition is also problematic in cancer metastasis, so the diminution of EMT with recombinant DNA could have great implications in future cancer treatment options. [ 9 ] BMP7 administration has been proposed as a possible treatment for human infertility due to poor response to FSH treatment.
Unlike epithelial cells – which are stationary and characterized by an apico-basal polarity with binding by a basal lamina, tight junctions, gap junctions, adherent junctions and expression of cell-cell adhesion markers such as E-cadherin, [4] mesenchymal cells do not make mature cell-cell contacts, can invade through the extracellular matrix, and express markers such as vimentin ...
The activation of these pathways result in increased proliferation, invasion and migration of BCSCs. As a result, primary breast cancer tumors quickly form metastases in distant sites. Both the epithelial-to-mesenchymal transition (EMT) and the mesenchymal-to-epithelial transition (MET) are key components of driving this metastasis process.
Cytokeratin-negative CTCs are characterised by the lack of EpCAM or cytokeratins, which may indicate an undifferentiated phenotype (circulating cancer stem cells) or the acquisition of a mesenchymal phenotype (known as epithelial-mesenchymal transition or EMT). These populations of CTCs may be the most resistant and most prone to metastasis.
Wnt signaling is involved in another key migration process known as the epithelial-mesenchymal transition (EMT). This process allows epithelial cells to transform into mesenchymal cells so that they are no longer held in place at the laminin. It involves cadherin down-regulation so that cells can detach from laminin and migrate.
Together with TGF-β, an important role of β-catenin is to induce a morphogenic change in epithelial cells. It induces them to abandon their tight adhesion and assume a more mobile and loosely associated mesenchymal phenotype. During this process, epithelial cells lose expression of proteins like E-cadherin, Zonula occludens 1 (ZO1), and ...
[3] [4] In addition, this cell line has a low expression of the Ki-67 proliferation marker, down regulation of claudin-3 and claudin-4, enrichment for markers associated with the epithelial-mesenchymal transition and the CD44+ CD24-/low phenotype associated with breast cancer stem cells and increased metastasis, [5] [6] [7] and is a mutant in ...