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In support of this model, Mostov and colleagues have identified the effects of HGF on MDCK acini as eliciting a partial transition from epithelial to mesenchymal cell phenotypes. [25] This argument marshals an established signaling program termed the epithelial to mesenchymal transition (EMT), by which sessile epithelial cells become motile and ...
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 ...
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 ...
Similar to collective cell migration in development and wound healing, cancer cells also undergo epithelial to mesenchymal transition (EMT), that reduces cell-cell adhesions and allows cancer spreading. [20] The diagram on the right shows: A: Border cell migration in a Drosophila embryo. (a) shows border cells migrating in a confined space ...
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.
Currently, three main theories have been proposed to explain the metastatic pathway of cancer: the epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) hypothesis (1), the cancer stem cell hypothesis (2), and the macrophage–cancer cell fusion hybrid hypothesis (3).
By studying the mesenchymal-epithelial transition (MET) process in which fibroblasts are pushed to a stem-cell like state, Ding's group identified two chemicals – ALK5 inhibitor SB431412 and MEK (mitogen-activated protein kinase) inhibitor PD0325901 – which was found to increase the efficiency of the classical genetic method by 100 fold.
Epithelial cell adhesion molecule (EpCAM), also known as CD326 among other names, is a transmembrane glycoprotein mediating Ca 2+-independent homotypic cell–cell adhesion in epithelia. [5] EpCAM is also involved in cell signaling, [ 6 ] migration, [ 7 ] proliferation, and differentiation. [ 8 ]