Interactions between cancer cells and the endothelium in metastasis

Orr, F. W.; Wang, H. Helen; Lafrenie, Robert M.; Scherbarth, Sandra; Nance, Dwight M.

doi:10.1002/(sici)1096-9896(200002)190:3<310::aid-path525>3.0.co;2-p

Cited by 253 publications

(153 citation statements)

References 113 publications

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“…Our results show that the location of the binding is very specific, with all the PC3-GFP cells binding at endothelial cell junctions. It has been shown that prostate epithelial cells interact directly with the BME cells, initially via selectins and this interaction is then stabilised by integrin binding (Orr et al, 2000). These are not the only binding steps, since antibodies to CD11a, CD18, LFA-1 and CD31 have also been shown to interfere with the binding process (Lehr and Pienta, 1998).…”

Section: Discussionmentioning

confidence: 99%

Invasive characteristics of human prostatic epithelial cells: understanding the metastatic process

et al. 2005

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Prostate cancer has a predilection to metastasise to the bone marrow stroma (BMS) by an as yet uncharacterised mechanism. We have defined a series of coculture models of invasion, which simulate the blood/BMS boundary and allow the elucidation of the signalling and mechanics of trans-endothelial migration within the complex bone marrow environment. Confocal microscopy shows that prostate epithelial cells bind specifically to bone marrow endothelial-to-endothelial cell junctions and initiate endothelial cell retraction. Trans-endothelial migration proceeds via an epithelial cell pseudopodial process, with complete epithelial migration occurring after 232743 min. Stromal-derived factor-1 (SDF-1)/CXCR4 signalling induced PC-3 to invade across a basement membrane although the level of invasion was 3.5-fold less than invasion towards BMS (P ¼ 0.0007) or bone marrow endothelial cells (P ¼ 0.004). Maximal SDF-1 signalling of invasion was completely inhibited by 10 mM of the SDF-1 inhibitor T140. However, 10 mM T140 only reduced invasion towards BMS and bone marrow endothelial cells by 59% (P ¼ 0.001) and 29% (P ¼ 0.011), respectively. This study highlights the need to examine the potential roles of signalling molecules and/or inhibitors, not just in single-cell models but in coculture models that mimic the complex environment of the bone marrow.

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Section: Discussionmentioning

confidence: 99%

Invasive characteristics of human prostatic epithelial cells: understanding the metastatic process

et al. 2005

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“…A variety of integrins have been found to be expressed by tumor cells and, depending on the degree of the tumor differentiation, some integrins may be up-regulated or down-regulated (111). The overexpression of integrins is thought to cause constitutive activation of signaling pathways leading to increased growth of tumor cells (112)(113)(114).…”

Section: The Role Of Osteopontin In Cancermentioning

confidence: 99%

The Role of Osteopontin in Tumor Progression and Metastasis in Breast Cancer

Rodrigues

Teixeira

Schmitt

et al. 2007

Cancer Epidemiology, Biomarkers &Amp; Prevention

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The use of cancer biomarkers to anticipate the outlines of disease has been an emerging issue, especially as cancer treatment has made such positive steps in the last few years. Progress in the development of consistent malignancy markers is imminent because advances in genomics and bioinformatics have allowed the examination of immense amounts of data. Osteopontin is a phosphorylated glycoprotein secreted by activated macrophages, leukocytes, and activated T lymphocytes, and is present in extracellular fluids, at sites of inflammation, and in the extracellular matrix of mineralized tissues. Several physiologic roles have been attributed to osteopontin, i.e., in inflammation and immune function, in mineralized tissues, in vascular tissue, and in kidney. Osteopontin interacts with a variety of cell surface receptors, including several integrins and CD44. Binding of osteopontin to these cell surface receptors stimulates cell adhesion, migration, and specific signaling functions. Overexpression of osteopontin has been found in a variety of cancers, including breast cancer, lung cancer, colorectal cancer, stomach cancer, ovarian cancer, and melanoma. Moreover, osteopontin is present in elevated levels in the blood and plasma of some patients with metastatic cancers. Therefore, suppression of the action of osteopontin may confer significant therapeutic activity, and several strategies for bringing about this suppression have been identified. This review looks at the recent advances in understanding the possible mechanisms by which osteopontin may contribute functionally to malignancy, particularly in breast cancer. Furthermore, the measurement of osteopontin in the blood or tumors of patients with cancer, as a way of providing valuable prognostic information, will be discussed based on emerging clinical data. (Cancer Epidemiol Biomarkers Prev 2007;16(6):1087 -97)

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“…Morphological studies suggest that cancer cells invade into the blood stream mainly via small veins or the sinusoidal neovasculature of their parent tumor (Orr et al, 2000). This process involves the degradation of the extracellular matrix and of the basement membrane by cancer cell-as well as host cell-derived enzymes (Meyer and Hart, 1998;Wandel et al, 2000Wandel et al, , 2002.…”

Section: Introductionmentioning

confidence: 99%

Interaction of human Thy-1 (CD 90) with the integrin αvβ3 (CD51/CD61): an important mechanism mediating melanoma cell adhesion to activated endothelium

et al. 2005

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The expression of the avb3 integrin (CD51/CD61) on human melanoma cells has been shown to be associated most closely with tumor progression and metastases formation in melanoma. Here, we demonstrated a specific interaction of the avb3 integrin on melanoma cells with the human Thy-1, an inducible cell adhesion molecule expressed on the cell surface of activated endothelial cells (EC). The interaction was shown by the binding of purified Thy-1 protein to a V b 3 transfected cells, to avb3-expressing melanoma cells and to purified a V b 3 integrin. Moreover, melanoma cells adhere specifically to Thy-1 transfectants via avb3 on melanoma cells showing the functional relevance of this interaction for cell adhesion. Finally, the importance of the avb3/Thy-1 interaction for the adhesion of melanoma cells to the activated endothelium was confirmed under static and flow conditions by the inhibition of melanoma cell adhesion to and transmigration across activated EC by blocking the avb3/Thy-1 interaction. In conclusion, we have identified a new pair of adhesion molecules Thy-1 and avb3 mediating the interaction of melanoma cells and activated EC. These data explain at least in part the high tumorigenicity of avb3-expressing melanoma cells and the association of avb3-positive melanoma cells with a high risk of metastasis and poor prognosis.

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Interactions between cancer cells and the endothelium in metastasis

Cited by 253 publications

References 113 publications

Invasive characteristics of human prostatic epithelial cells: understanding the metastatic process

Invasive characteristics of human prostatic epithelial cells: understanding the metastatic process

The Role of Osteopontin in Tumor Progression and Metastasis in Breast Cancer

Interaction of human Thy-1 (CD 90) with the integrin αvβ3 (CD51/CD61): an important mechanism mediating melanoma cell adhesion to activated endothelium

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