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Query: UMLS:C0001511 (Adhesion)
5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A very simple, rapid and reproducible method has been developed for studying the interaction of lectins with the cell surface. This involves determining the number of adherent cells after shaking cell suspensions in Petri dishes which have had a lectin coupled to their surface using 1-cyclohexyl-3-(2-morpholinoethyl) carbodiimide metho-p-toluene sulfonate. Using concanavalin A coupled to 60 mm diameter dishes and between 1.5 and 2 x 10(6) tumour cells, this adhesion reached a maximum after 10 min shaking. Maximum cell adhesion also varied according to the particular lectin used. Adhesion was absent or was very low if cells were shaken in untreated dishes, or in dishes coupled to bovine serum albumin, or in the presence of the lectin-specific sugar-competitor. Under conditions of maximum cell adhesion, the binding of two different lymphosarcoma lines to four different lectins was very similar, whereas the binding of a carcinoma line to these lectins was completely different from that observed for the lymphosarcomas.
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PMID:A simple lectin-mediated cell-adhesion method for investigating the cell surface. 58 40

To identify adhesion molecules involved in the formation of liver metastases, we prepared monoclonal antibodies against rat liver plasma membranes, that inhibited the adhesion of mouse metastatic TA3 mammary carcinoma cells to rat hepatocytes in vitro. Two such antibodies (designated OPAR-1 and OPAR-2) were obtained, that inhibited by over 70%. As assessed with gel electrophoresis and immunoblotting, these antibodies bound predominantly to plasma membrane proteins with molecular weights of 125,000 and 100,000. Using immunoelectron microscopy, the OPAR antigen was found to be abundantly present on the sinusoidal surface of hepatocytes, and in addition on contiguous hepatocyte surfaces and Kupffer cells, but was absent from sinusoidal endothelial cells. The tissue distribution and molecular weight indicate that the OPAR antigen is different from other hepatic adhesion molecules. Adhesion of MB6A lymphosarcoma cells was not inhibited by OPAR antibodies, indicating that these cells adhere to hepatocytes via a different surface molecule.
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PMID:Hepatocyte surface molecule involved in the adhesion of TA3 mammary carcinoma cells to rat hepatocyte cultures. 401 53

Mechanisms of adhesion between tumor cells and hepatocytes, which are likely to play a role in liver metastasis formation, were studied in vitro. TA3 mammary carcinoma and MB6A lymphosarcoma cells were added to rat hepatocytes that had been cultured for 24 hours. Adhesion was quantified by counting adherent cells seen in sections of pelleted, Epon-embedded culture fragments. Adhesion of TA3, but not of MB6A cells, was inhibited by antibodies prepared from an antiserum raised against sinusoidal face-enriched liver plasma membranes. Detergent-solubilized liver components, affinity purified on immobilized inhibitory antibodies, neutralized inhibition, whereas a subfraction separated from this material with the use of immobilized noninhibitory antiliver antibodies had no neutralizing activity. Adhesion of MB6A but not of TA3 cells was inhibited by the calcium ionophore A23187 and the local anesthetic procaine. The calmodulin inhibitor trifluoperazine inhibited adhesion of MB6A cells more strongly than that of TA3 cells. Finally, adhesion of TA3 cells was dependent on external calcium, whereas in the case of MB6A cells calcium could be replaced by magnesium. These observations suggested that adhesion of the two tumor cell types to hepatocytes involved distinct hepatocyte surface molecules and required distinct biochemical machinery.
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PMID:Adhesion of tumor cells to hepatocytes: different mechanisms for mammary carcinoma compared with lymphosarcoma cells. 643 81