39 Co-ordinate overexpression of urokinase receptor and αvβ5 vitronectin receptor in breast cancer

Carriero, Maria Vincenza; Vecchio, Silvana Del; Franco, Paola; Capozzoli, Monica; Corvino, L.; Potena, M. I.; Zannetti, Antonella; Stoppelli, Maria Patrizia; Salvatore, Marco

doi:10.1016/s0268-9499(97)80154-3

Cited by 12 publications

(16 citation statements)

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“…The data of Table 1 also con®rmed that antiavb3 antibodies inhibit pro-uPA stimulation of chemotaxis as previously published (Degryse et al, 1999) and suggested some kind of association between uPAR and avb3 integrin in RSMC. This is not surprising since interactions of uPAR with integrins have been observed in several cell types (Bohuslav et al, 1995;Wei et al, 1996;Yebra et al, 1996;Xue et al, 1997;May et al, 1998;Chavakis et al, 1998;Carriero et al, 1999;Simon et al, 2000). Direct interactions between uPAR and avb3 has also been reported (Tarui et al, 2000).…”

Section: Vn and Pro-upa Have Additive Effects On Rsmc Migrationmentioning

confidence: 85%

“…In addition to their direct involvement in the proteolytic (uPAR) and adhesive properties of cells, both pro-uPA (Gudewicz and Bilboa, 1987; Boyle et Fibbi et al, 1988;Del Rosso et al, 1992;Resnati et al, 1996;Gyetko et al, 1996;Degryse et al, 1999) and VN (Yebra et al, 1996;Kjùller et al, 1997;Stahl and Mueller, 1997;Carriero et al, 1999; directly stimulate cell migration. The interaction of uPAR with several integrins and the modulation of their function is an established fact; for example, the presence and the level of uPAR a ects the choice between adhesion on ®bronectin v. vitronectin, the internalization of ®brinogen or even the constitutive activation of MAP-K in certain cancer cells leading to cell proliferation Simon et al, 1996;Xue et al, 1997;Dumler et al, 1999;Aguirre Ghiso et al, 1999;Kusch et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…The interaction of uPAR with several integrins and the modulation of their function is an established fact; for example, the presence and the level of uPAR a ects the choice between adhesion on ®bronectin v. vitronectin, the internalization of ®brinogen or even the constitutive activation of MAP-K in certain cancer cells leading to cell proliferation Simon et al, 1996;Xue et al, 1997;Dumler et al, 1999;Aguirre Ghiso et al, 1999;Kusch et al, 2000). Direct interactions of uPAR with integrins has been shown by several techniques, including¯uorescence resonance energy transfer and co-immuno-precipitation (Bohuslav et al, 1995;Wei et al, 1996;Yebra et al, 1996;Xue et al, 1997;Carriero et al, 1999Simon et al, 2000. Speci®cally, association of uPAR with a v b 3 -expressing cells has also been reported (Tarui et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

“…Interactions between uPAR and integrins has been demonstrated in a variety of examples (Bohuslav et al, 1995;Wei et al, 1996;Yebra et al, 1996;Carriero et al, 1999). A speci®c direct uPAR-binding sequence has been identi®ed in the a4 chain subunit of integrins (Simon et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

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Urokinase/urokinase receptor and vitronectin/αvβ3 integrin induce chemotaxis and cytoskeleton reorganization through different signaling pathways

et al. 2001

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Vitronectin (VN) and pro-urokinase (pro-uPA) stimulated migration of rat smooth muscle cells in a dosedependent and additive way, and induced motile-type changes in cell morphology together with a complete reorganization of the actin ®laments and of the microtubules. All these e ects were inhibited by pertussis toxin, or by antibodies directed against the urokinase receptor (uPAR) or against the VN receptor a v b 3 suggesting that an association between the two receptors is required to mediate both signals. Investigation of the signaling pathways showed that increasing the intracellular cAMP resulted in a selective inhibition of VNinduced cell migration. On the other hand, PD 98059, an inhibitor of MEK, di erentially inhibited the pro-uPAbut not the VN-induced cell migration. Phosphorylation and nuclear translocation of Erk by pro-uPA was directly observed. We conclude that the signaling pathways of pro-uPA and VN must be at least in part di erent. Oncogene (2001Oncogene ( ) 20, 2032Oncogene ( ± 2043

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Section: Vn and Pro-upa Have Additive Effects On Rsmc Migrationmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Urokinase/urokinase receptor and vitronectin/αvβ3 integrin induce chemotaxis and cytoskeleton reorganization through different signaling pathways

et al. 2001

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“…Individual spheroids were transferred to 96-well plates, incubated for 24 h, and then were fixed and stained with Hema-3 (e) Cell migration from the spheroids was measured with an ocular micrometer (f) uPA and PI3k/Akt in glioma N Chandrasekar et al between uPAR and integrins, which leads to potentiation of integrin-mediated signaling and enhanced cell migration (MacDonald et al, 1998;Yebra et al, 1999). Treatment of breast carcinoma cell lines with uPA has been shown to promote the physical association of uPAR with avb5, which is required for uPAR-directed cell migration; uPA has also been shown to promote cytoskeletal rearragements that are mediated by avb5 (Carriero et al, 1999). Our work with SNB19 cells shows that downregulation of uPA may decrease the occupancy of the uPAR and thereby the integrinmediated organization of the actin-containing cytoskeleton and the migration of the cells.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of uPA inhibits migration and PI3k/Akt signaling in glioblastoma cells

Chandrasekar

Mohanam

Gujrati³

et al. 2003

Oncogene

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The ability of glioma cells to migrate great distances from a primary tumor mass is the primary cause of tumor recurrence. The urokinase-type plasminogen activator (uPA) is a serine protease that can initiate proteolytic cascades, which result in remodeling of extracellular matrix and basement membrane, allowing cells to move across and through these barriers. The binding between uPA and its receptor uPAR also mediates several signaling events that seem to contribute to the evolution of a migratory phenotype. In this study, we determined how the downregulation of uPA affects the signaling pathways leading to cell migration. Stably transfecting human glioblastoma cells with antisense uPA decreased the amount of cell-bound uPA and disrupted actin cytoskeleton formation and cell migration. The phosphatidylinositol 3-kinase (PI3k) and Akt signaling pathway has been suggested to mediate migration in various cancer cells. The antisense-uPA clones also had less phosphorylated PI3k and Akt than control cells, a finding associated with decreased cell migration, G2/M-phase arrest, and decreased clonogenic survival. Decreased activation of PI3k and the antiapoptotic factor Akt was not sufficient to induce apoptosis in the antisense-uPA clones, but staurosporine sensitized them to apoptosis to a greater extent than control cells. These results indicate that PI3k/ Akt pathway is involved in the signaling cascade required to induce cell migration and that uPA has a direct role in regulating migration.

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PET/CT in cancer research: from preclinical to clinical applications

Vecchio

Zannetti

Fonti

et al. 2010

Contrast Media & Molecular

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The identification of genetic and biochemical mechanisms underlying tumor growth and progression along with the unraveling of human genoma provided a plethora of new targets for cancer detection, treatment and monitoring. Simultaneously, the extraordinary development of a number of imaging technologies, including hybrid systems, allowed the visualization of biochemical, molecular and physiological aberrations linked to underlying mutations in a given tumor. In vivo evaluation of complex biological processes such as proliferation, apoptosis, angiogenesis, metastasis, gene expression, receptor-ligand interactions, transport of substrates and metabolism of nutrients in human cancers is feasible using PET/CT and radiolabeled molecular probes. Some of these compounds are in preclinical phases of evaluation whereas others have been already applied in clinical settings. Here we provide prominent examples on how some biological processes and target expression can be visualized by PET/CT in animal tumor models and cancer patients for the noninvasive detection of well-known markers of tumor aggressiveness, invasiveness and resistance to treatment and for the evaluation of tumor response to therapy.

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39 Co-ordinate overexpression of urokinase receptor and αvβ5 vitronectin receptor in breast cancer

Cited by 12 publications

References 0 publications

Urokinase/urokinase receptor and vitronectin/αvβ3 integrin induce chemotaxis and cytoskeleton reorganization through different signaling pathways

Urokinase/urokinase receptor and vitronectin/αvβ3 integrin induce chemotaxis and cytoskeleton reorganization through different signaling pathways

Downregulation of uPA inhibits migration and PI3k/Akt signaling in glioblastoma cells

PET/CT in cancer research: from preclinical to clinical applications

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