Inverse relation of autocrine motility factor receptor and E-cadherin expression following MDCK epithelial cell transformation.
Autocrine motility factor interacts with its cell surface receptor (AMF-R) to stimulate tumor cell motility. To study AMF-R expression following transformation of polarized epithelial MDCK cells, we have used the invasive Moloney sarcoma virus transformed MDCK (MSV-MDCK) cell population. Decreased E-cadherin expression of the transformed MSV-MDCK clones is associated with both increased cellular motility and increased AMF-R expression. Increased AMF-R expression is due to MSV transformation as differentially motile MSV-MDCK clones, which either retain low E-cadherin, exhibit equivalent high levels of AMF-R. Loss of the polarized epithelial phenotype and increased cellular motility following transformation of MDCK cells is thus associated with a shift from a high E-cadherin/low AMF-R to a low E-cadherin/low AMF-R phenotype.
Simard
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Départements d'anatomie et de pathologie, Université de Montréal, Québec, Canada.
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D000818:Animals; D015820:Cadherins / Q000096:biosynthesis*; D002461:Cell Line, Transformed; D002465:Cell Movement; D002471:Cell Transformation, Neoplastic; D004285:Dogs; D015870:Gene Expression; D007365:Intercellular Junctions / Q000502:physiology / Q000648:ultrastructure; D007668:Kidney; D008980:Moloney murine sarcoma virus; D010641:Phenotype; D060285:Receptors, Autocrine Motility Factor; D018121:Receptors, Cytokine / Q000096:biosynthesis*; D044767:Ubiquitin-Protein Ligases
D015820:Cadherins; D018121:Receptors, Cytokine; D060285:Receptors, Autocrine Motility Factor; D044767:Ubiquitin-Protein Ligases