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

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.
Cancer Res 1985 Aug
PMID:Hepatocyte surface molecule involved in the adhesion of TA3 mammary carcinoma cells to rat hepatocyte cultures. 401 53

The rates of disaggregation of tumor and normal cells of the breast were studied. Intercellular bonds in tumor tissue were found to be weaker than in normal tissue. The expansion of cancer was in close correlation with the weakening of intercellular bonds in tumor tissue. Adhesion of tumor cells is an important factor of metastatic spread.
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PMID:[Relation of the degree of cancerous tissue disaggregation of the breast to the spread of the tumor process]. 631 58

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.
J Natl Cancer Inst 1984 Oct
PMID:Adhesion of tumor cells to hepatocytes: different mechanisms for mammary carcinoma compared with lymphosarcoma cells. 643 81

Microfilaments are known to participate in several cellular functions. Proteins which cross-link, sever or cap F-actin filaments, and those inhibit polymerization of G-actin may regulate intracellular distribution, length and amount of F-actin to cope with wide varieties of cellular functions of microfilaments. Actinogelin, a calcium-regulated crosslinking protein of F-actin, was discovered in and purified from Ehrlich tumor cells. Native molecule of the protein was found to be consisted of two 110,000-115,000 dalton subunits. Gelation of F-actin can be induced by the addition of the purified protein, and this can be inhibited by Ca2+ (half maximal inhibition, 2 microM). Actinogelin is distributed in several types of cells including fibroblasts, epithelial cells, macrophages and lymphocytes. This protein is found to localize at crossing or converging points of stress fibers (bundle of microfilaments) by immunofluorescence staining using anti-actinogelin antibody. Adhesion plaques of fibroblasts are also stained. Since oncogene product of Rous sarcoma virus, pp 60src, is also present in adhesion plaques, possible phosphorylation of actinogelin in a RSV-transformed cells was studied by the immunoblotting technique. It was found that phosphorylation of actinogelin occurred only at permissive temperature. This modification of the protein might be a cause of disappearance of stress fibers from cancer cells.
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PMID:[Regulatory proteins of the cytoskeleton system and their changes associated with carcinogenesis]. 668 52

Adhesion in vitro is described in cells from a tumor pair originating from a single methylcholanthrene-induced mouse carcinoma. One member of this tumor pair shows a high incidence of metastases while the other does not metastasize. Cells from the non-metastasizing carcinoma were found to form close and focal contacts with a glass substrate consecutively, as do normal mouse kidney epithelial cells. Cells from the metastasizing carcinoma, however, had only limited areas of close contact and generally failed to form focal contacts. It is suggested that this alteration in cell-substrate adhesion contributes to the release and mobility of metastatic cells.
Int J Cancer 1980 Nov 15
PMID:Adhesion of metastatic and non-metastatic carcinoma cells to glass surfaces. 723 23

Polyunsaturated fatty acids influence several steps involved in metastasis formation in animal tumor models. During the process of metastasis from the primary site, tumor cells adhere to the endothelium and underlying basement membrane before extravasation and secondary growth. The purpose of this study was to determine the effect of unsaturated fatty acids on adhesion of human breast cancer cell lines to components of the basement membrane. Cells were cultured in low-serum medium for five days with or without added unsaturated fatty acids. Adhesion assays were conducted by incubating cells with basement membrane substrates coated on 96-well plates, washing to remove nonadherent cells, and staining adherent cells with crystal violet. Linoleic acid (LA) and eicosapentaenoic acid increased adhesion of the metastatic cell line MDA-MB-231 to Matrigel and type IV collagen, while eicosapentaenoic acid decreased adhesion of the less metastatic cell line SK-BR-3 to these two basement membrane substrates. Oleic acid increased adhesion of MDA-MB-231 cells to Matrigel and fibronectin. Nordihydroguaiaretic acid and high concentrations of indomethacin, each of which inhibits the lipoxygenase pathway of arachidonate metabolism, were effective in reversing the stimulatory effect of LA on MDA-MB-231 cell adhesion. A protein kinase C inhibitor likewise suppressed the increase in adhesion observed when MDA-MB-231 cells were incubated in media with added LA. Unsaturated fatty acids modified the adhesive properties of human breast cancer cell lines in vitro, and LA appeared to increase human breast cancer cell adhesion to extracellular matrix components by activating lipoxygenase and/or protein kinase C pathways.
Nutr Cancer 1995
PMID:Unsaturated fatty acid effects on human breast cancer cell adhesion. 749 Dec 98

We have investigated the regulatory role of PGI2 and its stable analogs, i.e., iloprost and cicaprost, on 12(S)-HETE- and TPA-enhanced tumor cell integrin expression and adhesion. Walker 256 carcinosarcoma cells express alpha IIb beta 3 integrin receptors, which mediate their adhesion to endothelium, subendothelial matrix and fibronectin. Adhesion is enhanced by treatment with exogenous 12(S)-HETE but not 12(R)-HETE or other lipoxygenase-derived hydroxy fatty acids, as well as by TPA. Both 12(S)-HETE and TPA enhanced alpha IIb beta 3 expression on W256 cells. PGI2 iloprost and cicaprost inhibited both 12(S)-HETE- and TPA-enhanced adhesion to endothelium and subendothelial matrix as well as alpha IIb beta 3 expression on W256 cells. The mechanism responsible for the effect of PGI2 was explored. Prostacyclin treatment of W256 cells resulted in an enhanced production of cAMP in a time- and dose-dependent manner. Pre-treatment of tumor cells with increasing concentrations of adenosine resulted in a dose-dependent decrease in the PGI2 effect on TPA or 12(S)-HETE-enhanced adhesion, suggesting that the PGI2 effect is mediated through PKA. Dibutyryl cAMP also blocked the 12(S)-HETE- or TPA-enhanced adhesion, and adenosine pre-treatment did not result in an inhibition of the dibutyryl cAMP effect. Collectively, our results suggest that the cyclooxygenase metabolite PGI2 can antagonize the lipoxygenase metabolite 12(S)-HETE- and TPA-enhanced alpha IIb beta 3 expression and tumor cell adhesion via activation of adenylate cyclase and elevation of intracellular levels of cAMP.
Int J Cancer 1995 Jan 27
PMID:Inhibition of TPA and 12(S)-HETE-stimulated tumor cell adhesion by prostacyclin and its stable analogs: rationale for their antimetastatic effects. 753 Feb 35

Adhesion of cancer cells to endothelium is thought to be a prerequisite to extravasation during the haematogenous phase of metastasis, and is enhanced after perturbation of the endothelium by interleukin-1 (IL-1). The inducible endothelial adhesion molecules, E-selectin, VCAM-1/alpha 4 beta 1 and vitronectin receptor have been reported to mediate attachment of cancer cells to IL-1-treated endothelial cells. We have examined the relative contribution of these molecules by quantifying the adhesion of a panel of 22 human, 125I-labelled cancer cells and the rat W256 tumour to untreated and IL-1-treated endothelial monolayers in the presence of relevant neutralising antibodies. Antibodies against E-selectin inhibited the adhesion of HL-60 leukaemia cells and two colon carcinomas. Anti-alpha 4 beta 1 antibodies blocked adhesion of four melanomas, five sarcomas and one lung carcinoma. Anti-vitronectin receptor antibodies inhibited adhesion of 14 of the 22 human cell lines to IL-1-treated endothelial cells. Adhesion of seven cell lines was inhibited by more than a single antibody. In contrast, adhesion of one of the cancer cell lines was unaffected by any of the antibodies, suggesting involvement of other IL-1-inducible endothelial adhesion molecules. Moreover, none of the antibodies altered the attachment of cancer cells to unstimulated endothelial monolayers. We conclude that the mechanisms of cancer cell adhesion to the endothelium are influenced by endothelial activation and by the adhesive repertoire of the cancer cell.
Eur J Cancer 1994
PMID:The relative roles of vitronectin receptor, E-selectin and alpha 4 beta 1 in cancer cell adhesion to interleukin-1-treated endothelial cells. 753 92

Changes in glycoconjugate production have been reported for tumor cells. In this study, we investigated the glycoconjugate expression pattern in normal human melanocytes and in a panel of 6 human melanoma cell lines with different metastatic capacity after s.c. inoculation into nude mice. Glycoconjugates were labeled in vitro with [35S] sulphate and [3H] glucosamine, purified from cells and culture medium by column chromatography and identified by treatment with specific glycosidases. Characterization of the purified glycoconjugate fractions as well as alcian-blue staining of xenograft lesions revealed that hyaluronic acid (HA) is the main glycoconjugate produced by all cell lines. Highly metastatic cell lines expressed higher levels of HA than melanocytes and than weakly metastatic or non-metastatic cell lines. In addition, a shift in dominance from chondroitin-sulphate proteoglycan to heparan-sulphate proteoglycan was observed with increasing metastatic capacity. We also studied the expression and binding activity of the HA receptor CD44. Immunoprecipitation experiments indicated high CD44 synthesis only in highly metastatic cell lines, but FACS analysis demonstrated approximately the same surface expression in melanocytes as in all cell lines. Adhesion assays to immobilized HA showed that CD44 can be present in an inactive or an active conformation. Our data suggest that a combination of increased HA production and the expression of CD44 on the cell surface may be associated with high metastatic potential of human melanoma cell lines in nude mice.
Int J Cancer 1995 Apr 10
PMID:Glycoconjugate profile and CD44 expression in human melanoma cell lines with different metastatic capacity. 753 56

Interactions between tumour cells and the endothelium are vital to the formation of haematogenous metastases. Binding to model endothelium of one oestrogen receptor positive breast carcinoma cell line (MCF-7) and one receptor negative line (HS578T) was examined in vitro together with endothelial retraction induced by these tumour cells. Adhesion was inhibited by monoclonal antibodies specific for the VLA integrins and by peptides containing the RGD motif which is commonly recognised as a ligand by the VLA adhesion molecules. However, binding of the two tumour cell lines was inhibited by monoclonal antibodies specific for different VLA molecules; anti-alpha 6 beta 1 inhibited MCF-7 adhesion but anti-alpha 5 beta 1 inhibited Hs578T. These results were consistent with flow cytometric quantification of the expression of these VLA integrins on the surfaces of the two tumour cell lines. Enzyme-linked immunosorbent assays (ELISA) demonstrated that laminin was present on the endothelial cell surface but collagen IV was absent. ELISA failed to detect increased exposure of the subendothelial matrix during the first hour after addition of either cancer cell type. This was supported by assays which demonstrated maintenance of the endothelial permeability barrier during this period. Slight endothelial retraction was detected within 2 hours of the addition of tumour cells. It is concluded that binding between tumour cells and confluent endothelium is inhibited by the blockade of adhesion molecules which are normally associated with interactions between the cell and the subendothelial matrix. Tumour cell to matrix interactions rather than direct tumour to endothelial cell adhesion may be the limiting step in tumour cell binding to the endothelium.
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PMID:The role of beta 1 integrins in adhesion of two breast carcinoma cell lines to a model endothelium. 753 54


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