Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adhesion between monocytic and mesothelioma or pleural mesothelial cells influences stromal remodeling in pleural neoplasia. We found that cultured monocytic cells (U937) adhere to either human pleural mesothelioma (MS-1) or mesothelial (MeT5A) cells in vitro. 125I-fibrinogen bound specifically and saturably to either cell line, and specific fibrinogen binding increased upon stimulation of these cells with proinflammatory agents such as phorbol myristate (PMA), lipopolysaccharide (LPS) or tumor necrosis factor (TNF-alpha). We purified the fibrinogen receptor protein from a membrane fraction of MS-1 cells and identified it by immunoprecipitation as intercellular adhesion molecule (ICAM-1). Anti-ICAM-1 antibody or antisense oligonucleotides inhibited fibrinogen-mediated cell adhesion and binding of 125I-fibrinogen to mesothelioma or mesothelial cells. Cultured monocytic cells adhere to either mesothelioma or mesothelial cells, and the interaction is promoted by fibrinogen binding ICAM-1 at the cell surface. ICAM-1 is expressed by mesothelioma cells and CD 11b by macrophages in the fibrinous mesothelioma tumor stroma. The data suggest a common mechanism by which monocytic cells could adhere to either malignant mesothelioma cells or the mesothelial surface in pleural neoplasia.
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PMID:Fibrinogen promotes adhesion of monocytic to human mesothelioma cells. 872 24

Mesothelial cells (MC) form a polarized monolayer lining serosal cavities. During serositis, the MC lining undergoes hyperplasia, and MC are shed into effusions. During these processes, contact with basement membrane and, ultimately, neighboring cells is at least temporarily lost, suggesting regulated alterations in cell/matrix and cell/cell adhesion. Such interactions are primarily mediated by integrins. Malignant mesothelioma has a growth pattern characterized by lateral, limited invasive but contiguous spread. During serositis, activated MC, both sessile and detached, expressed an extended spectrum of beta1, beta3 and beta4 integrins compared with resting MC, as shown by immunohistology. Malignant mesothelioma had an integrin repertoire and a subcellular distribution resembling that of activated sessile rather than floating MC. In vitro, MC exposed a more comprehensive pattern of integrins than that of the newly established mesothelioma cell lines ME-HD-1 and ME-HD-2, as shown by flow cytometry. MC consistently adhered better than mesothelioma cells to laminin, tenascin, fibronectin and collagen type IV. Adhesion of MC and mesothelioma cells to these matrix proteins was, at least in part, mediated via beta1 integrins. The different integrin profiles and adhesion properties of cultured MC and mesothelioma cells may reflect a limited functional differentiation of the latter.
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PMID:Pleural mesothelioma mimics the integrin profile of activated, sessile rather than detached mesothelial cells. 921 27