Role of Tumour Cell Eicosanoids and Membrane Glycoproteins IRGPIb and IRGPIIb/IIIa in Metastasis

Honn, Kenneth V.; Grossi, Irma M.; Chopra, Hemi; Steinert, Bruce W.; Onoda, James M.; Nelson, Kevin; Taylor, John D.

doi:10.1007/978-3-642-73424-3_4

Cited by 8 publications

(18 citation statements)

References 32 publications

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“…Unexpectedly, tumor cell adhesion to EC was inhibited by about 50% by antietlIb~33 [107], strongly suggesting that activated tumor cell adhesion to EC is, at least partly, mediated by tumor cell integrin ctlIbf33. This result is in accord with the experimental findings of our own [76,[130][131][132][133]141]. Tumor cells activated by the lipoxygenase metabolite of arachdonic acid 12(S)-HETE [12(S)-hydroxyeicosatetraenoic acid], or by the phorbol ester TPA, demonstrated enhanced adhesion to microvascular EC, intact subendothelial matrix or to fibronectin [141].…”

Section: Tumor Ceii-ec Interactions and 'Docking And Locking' Hypothesissupporting

confidence: 93%

Adhesion molecules and tumor cell interaction with endothelium and subendothelial matrix

1992

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Cancer metastasis poses the greatest challenge to the eradication of malignancy. The majority of clinical and experimental evidence indicates that metastasis is a non-random, organ-specific process. Tumor cell interaction with endothelium and subendothelial matrix constitutes the most crucial factor in determining the organ preference of metastasis. A plethora of cell surface adhesion molecules, which encompass four major families (i.e., integrins, cadherins, immunoglobulins and selectins) and many other unclassified molecules, mediate tumor-host interactions. Adhesion molecules and adhesion processes are involved in most, if not all, of the intermediate steps of the metastatic cascade. Decreased E-cadherin expression and increased CD44 expression are clearly correlated with the acquisition of the invasive capacity of primary tumor cells. Similarly, altered expression pattern of many other adhesion molecules such as upregulated expression of the laminin receptors and depressed expression of fibronectin receptors (alpha 5 beta 1) appears to be involved in tumor cell invasion into the subendothelial matrix. Tumor cell-endothelium interactions involve several well-defined sequential steps that can be analyzed by the 'Docking and Locking' hypothesis at the molecular level. Tumor cell-matrix interactions are determined by the repertoire of adhesion receptors of tumor cells and the unique composition of organ-specific matrices. Our experimental data, together with others', suggest that the integrin alpha IIb beta 3 is one of the major players in these tumor-host interactions. Tumor-host interaction is a dynamic process which is constantly modulated by a host of factors including various cytokines, growth factors and arachidonate metabolites such as 12(S)-HETE. Delineation of the molecular mechanisms of tumor-host interactions may provide additional means to intervene in the metastatic process.

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Section: Tumor Ceii-ec Interactions and 'Docking And Locking' Hypothesissupporting

confidence: 93%

Adhesion molecules and tumor cell interaction with endothelium and subendothelial matrix

1992

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“…IRGpIb) and immunologically related GpIIb/IIIa (i.e. In contrast, human and rodent cancer cells do demonstrate decreased binding of GpIIb/IIIa complexdirected monoclonal antibodies in the presence of EDTA [27,87,88], consistent with their similarity to platelet GpIIb/IIIa. Immunological evidence has been reported for the presence of IRGpIb and IRGplIb/IIIa on human colon carcinoma (close A), human cervical carcinoma (MS751), rat Walker 256 carcinosarcoma, murine B16 amelanotic melanoma and Lewis lung carcinoma cancer cells [27,82,88,90].…”

Section: Adhesion and Adhesive Macromoleculesmentioning

confidence: 93%

“…These glycoproteins have been termed immunologically related GpIb (i.e. Endothelial cells (which possess the vitronectin receptor [52]) do not demonstrate decreased binding of complex-directed mAb7E3 in the presence of EDTA or calcium CaZ+-Mg2+-deficient media [27,87], consistent with the calcium independence of the vitronectin receptor complex. IRGpIIb/IIIa) [82].…”

Section: Adhesion and Adhesive Macromoleculesmentioning

confidence: 99%

“…At least one of those adhesive proteins (i.e. Human and rodent cancer cells treated with polyclonal and monoclonal antibodies to GpIIb/IIIa, but not antibodies against unrelated antigens, demonstrate partial to complete inhibition of their ability to induce platelet aggregation [27,87,89], suggesting that IRGpIIb/IIIa may serve as an adhesion site for platelet attachment to the cancer cell plasma membrane (see below). von Willebrand factor, fibronectin and vitronectin) are components of the subendothelial matrix.…”

Section: Adhesion and Adhesive Macromoleculesmentioning

confidence: 99%

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Interactions between cancer cells and the microvasculature: a rate-regulator for metastasis

1989

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Hematogenous metastasis is a major consideration in the staging, treatment and prognosis of patients with cancer. Key events affecting hematogeneous metastasis occur in the microvasculature. This is a brief, selective review of some interactions involving cancer cells and the microvasculature in pathologic sequence, specifically: (1) intravasation of cancer cells; (2) the arrest of circulating cancer cells in the microvasculature; (3) cancer cell trauma associated with arrest; (4) microvascular trauma; (5) the inflammatory; and (6) the hemostatic coagulative responses associated with arrest, and finally (7) angiogenesis, leading to tumor vascularization. The evidence shows that through a series of complex interactions with cancer cells, the microvasculature acts as a rate-regulator for the metastatic process, in addition to providing routes for cancer cell dissemination and arrest sites for cancer cell emboli.

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“…LOX activity is also altered. One LOX metabolite, 12(S)-hydroxyeicosatetraenoic acid (HETE), has been found to promote tumor cell adhesion and stimulate metastasis by augmenting the metastatic potential [44,45]. A positive correlation was found between 8(S)-HETE, another metabolite of LOX, hypoproliferation and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced tumor development [46].…”

Section: Sulindac and Its Metabolitesmentioning

confidence: 94%

A Review of Cancer Chemopreventive Agents

Levi¹,

Borne²,

Williamson³

2001

CMC

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In the late 20(th) century, the treatment of cancer began to include its prevention. Today, compounds exist that will lower the risk of developing certain types of cancer. This has been demonstrated in studies where chemically induced tumor growth has been slowed or reversed. Anti-inflammatory compounds having chemopreventive activity are piroxicam, sulindac, aspirin, celecoxib and curcumin. The selective estrogen receptor modulators, tamoxifen and raloxifene, are beneficial in the prevention of estrogen dependent tumors. Retinoids, vitamin A derivatives, such as targretin and fenretinide are useful in the prevention of tumors. Compounds containing sulfur, such as sulforaphane and oltipraz, are even useful as radioprotective agents. The steroid dehydroepiandosterone can inhibit experimental carcinogenesis. All of these chemical classes provide a start for the medicinal chemist to design more effective chemopreventive agents. The biomarkers used to determine the chemopreventive activity of new compounds are quite often activities of enzymes. The identification of those individuals at high risk is still in its infancy and presents a troubling dilemma.

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Role of Tumour Cell Eicosanoids and Membrane Glycoproteins IRGPIb and IRGPIIb/IIIa in Metastasis

Cited by 8 publications

References 32 publications

Adhesion molecules and tumor cell interaction with endothelium and subendothelial matrix

Adhesion molecules and tumor cell interaction with endothelium and subendothelial matrix

Interactions between cancer cells and the microvasculature: a rate-regulator for metastasis

A Review of Cancer Chemopreventive Agents

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