53 research outputs found
Molecular mechanisms leading to loss of differentiation and gain of invasiveness in epithelial cells
Mutation of juxtamembrane tyrosine residue 1001 suppresses loss-of-function mutations of the met receptor in epithelial cells
Different proliferative responses of periportal and pericentral rat hepatocytes to hepatocyte growth factor
The motility signal of scatter factor /hepatocyte growth factor mediated through the receptor tyrosine kinase Met requires intracellular action of Ras
Scatter factor/hepatocyte growth factor and its receptor, the c-met tyrosine kinase, can mediate a signal exchange between mesenchyme and epithelia during mouse development
Scatter factor/hepatocyte growth factor (SF/HGF) has potent motogenic, mitogenic, and morphogenetic activities on epithelial cells in vitro. The cell surface receptor for this factor was recently identified: it is the product of the c-met protooncogene, a receptor-type tyrosine kinase. We report here the novel and distinct expression patterns of SF/HGF and its receptor during mouse development, which was determined by a combination of in situ hybridization and RNase protection experiments. Predominantly, we detect transcripts of c-met in epithelial cells of various developing organs, whereas the ligand is expressed in distinct mesenchymal cells in close vicinity. In addition, transient SF/HGF and c-met expression is found at certain sites of muscle formation; transient expression of the c-met gene is also detected in developing motoneurons. SF/HGF and the c-met receptor might thus play multiple developmental roles, most notably, mediate a signal given by mesenchyme and received by epithelial. Mesenchymal signals are known to govern differentiation and morphogenesis of many epithelia, but the molecular nature of the signals has remained poorly understood. Therefore, the known biological activities of SF/HGF in vitro and the embryonal expression pattern reported here indicate that this mesenchymal factor can transmit morphogenetic signals in epithelial development and suggest a molecular mechanism for mesenchymal epithelial interactions
Molecular mechanisms leading to cell junction (cadherin) deficiency in invasive carcinomas
It has been realized for some time that the loss of epithelial differentiation in carcinomas, which is accompanied by higher mobility and invasiveness of the tumor cells, is a consequence of reduced intercellular adhesion. A variety of recent reports have indicated that the primary cause for the 'scattering' of the cells in invasive carcinomas is a loss of the integrity of intercellular adherens junctions often involving loss of a functional cell-cell adhesion molecule E-cadherin. In the present review, permanent and transient molecular mechanisms are discussed which lead to the impairment of junctional integrity of cells and thus the progression of carcinomas toward a more metastatic state
Tyrosine kinase receptors in the control of epithelial growth and morphogenesis during development
Properties and functions of scatter factor/hepatocyte growth factor and its receptor c-Met
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