Podoplanin expression in breast cancer cells induces cell migration and invasion with the formation of filopodia and simultaneous retention of Ecadherin expression.Data have been reported indicating that collectively migrating cancer cells can use the ability of adjacent mesenchymal cells to modify the structure of the matrix and rebuild it, and then follow in their “footsteps.” In in vitro experiments, the introduction of fibroblasts in the culture induces collective tumor cell migration to the underlying matrix in the form of chains. During carcinogenesis, epithelial cells are subjected to a morphological transformation that is phenotypically similar to EMT but develops in the absence of the relevant HGF ligand. The mesenchymal mechanism of invasion is believed to be the consequence of EMT, when active dedifferentiation of a malignant epithelial tumor occurs, and multicellular groups start to divide into single tumor cells, gaining a mesenchymal phenotype.A number of researchers have stressed that tumor cells during the mesenchymal type of migration go through a number of specific sequential steps that constitute a five-stage model of migration. This results in disruption in strong cadherin junctions and activation of polar cell migration and proteolysis of extracellular matrix components by various secreted proteases, with the functions of integrin receptors being retained. Aceasta este o categorie de redirecționare către categoria Cascade din România. Determination of the invasion mechanism used by single migrating cells during migration is a complex task. For example, amoeboid migration of tumor cells in the lymphatic and circulatory systems is considered as migration in a soft matrix.Condeelis and Segall elucidated some features of cell migration on the example of two different tumor lines, MTC and MTLn3, under in vitro and in vivo conditions. Similar results were obtained in studies of malignant tumors in vivo.

The cells have often developed resistance to several lines of previous treatment and have acquired special properties that permit them to metastasize to distant sites. Once the cancerous tissue is examined under a microscope to determine the cell type, a doctor can usually tell whether that type of cell is normally found in the part of the body from which the tissue sample was taken.

have indicated that EMT develops due to the induction of programs associated with the activation of key transcription factors, such as TWIST1, Snail, Slug, and ZEB1/2. Therefore, fibroblasts are a “guide” for invading tumor cells, remodeling the surrounding extracellular matrix to pathways with thick collagen bundles on the sides and a lack of a matrix in the center.LIM-kinase, a member of one of the protein families, plays a role in the development of collective migration by tumor cells.

Currently, EMT is known to underlie the processes of embryogenesis and inflammation and regeneration of tissues and, certainly, plays a key role in the mechanisms of carcinogenesis.Tumor cells spreading into the surrounding tissues and distant organs are known to reproduce the mechanisms and migration types characteristic of normal, non-tumor cells during physiological processes. The most common reasons for a patient with metastatic breast carcinoma to be treated with radiotherapy are: This is largely due to the fact that migrating cells temporarily lose their ability to divide. In addition, cells in the EMT state are known to also exhibit chemoresistance. The mechanisms that could underlie the described changes remain unclear.Tumor cells within a single tumor can simultaneously move both collectively and individually. Developing changes in the cell shape are generated by the cortical actin cytoskeleton that is, in turn, controlled by small GTPase RhoA and its effector, ROCK kinase. In this regard, some researchers describe the so-called partial EMT, in which most cells in the invasive front are involved (Fig. Particular attention has been paid to the phenotypic diversity of the primary tumor in invasive carcinoma of no special type, which accounts for the bulk (80%) of all histological types of breast cancer.Despite the considerable structural diversity of the primary breast tumor, five main types of morphological structures can be distinguished: alveolar, trabecular, tubular and solid structures, and discrete groups of tumor cells (Fig. In turn, the latter, in particular cells that have undergone EMT, are capable under certain conditions of gaining an epithelial phenotype and forming tumor multicellular complexes. 1). The growth of a new network of blood vessels, called tumor A recent study shows that PKC-iota promotes melanoma cell invasion by activating Vimentin during EMT. TGF-β is supposed to be a key regulator of the interactions between the tumor and stroma, which promotes collective cell migration in breast cancer.It has been established that leader cells express podoplanin, a transmembrane glycoprotein that is expressed under normal conditions in kidney podocytes, type 1 lung alveolar cells, skeletal muscle cells, placenta, etc.

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