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Rudroff, Claudia; Seibold, Stefan; Kaufmann, Roland; Zetina, Cecilia Cu; Reise, Kathrin; Schäfer, Ute; Schneider, Annette; Brockmann, Michael; Scheele, J.; Neugebauer, Edmund

doi:10.1023/a:1014598904644

Cited by 38 publications

(8 citation statements)

References 33 publications

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“…Overall changes in integrin and BMP‐4 and ligand‐independent down‐regulation of DAP‐3 [34–36] could also account for the previously observed inhibition of invasion observed after reintroduction of ERα [9]. Other events such as down‐regulation of thrombin receptor and up‐regulation of thrombomodulin could also account for the decreased invasiveness of these cells [37–39]. In addition, the down‐regulation of CTGF, which promotes angiogenesis [40], suggests that ERα exogenous expression could reduce the angiogenesis events during tumor formation.…”

Section: Discussionmentioning

confidence: 89%

Identification of genes involved in growth inhibition of breast cancer cells transduced with estrogen receptor

et al. 2003

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Estrogen receptor K K (ERK K)-negative breast cancer cells display an aggressive phenotype. We previously showed that adenoviral expression of ERK K in ER-negative breast cancer cells leads to an estrogen-dependent down-regulation of the proliferation, which could be of interest to control the growth of such cells. In this study, we observed an increase in protein levels of p21 and p27 cyclin-dependent kinase inhibitors, whereas pRb phosphorylation is strongly decreased. Flow cytometry experiments showed a slower transit of cells in G1 (hormoneindependent), a hormone-induced accelerated transit through S phase and a possible arrest in G2/M phase. In addition, ERK Kexpressing cells were undergoing apoptosis. By using cDNA macroarrays, we identi¢ed a novel collection of genes regulated by liganded ERK K potentially regulating cell cycle, apoptosis, cell signalling, stress response and DNA repair.

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Section: Discussionmentioning

confidence: 89%

Identification of genes involved in growth inhibition of breast cancer cells transduced with estrogen receptor

et al. 2003

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“…In addition to its well-recognized roles in platelet and vascular biology, PAR1 has been proposed to be involved in the invasive and metastatic processes of breast cancer (36, 37), pancreatic cancer (38), and melanoma (39–41) and has been identified as an oncogene in the transformation of NIH3T3 mouse fibroblasts (42, 43). PAR1 can stimulate Gα i , Gα q , and Gα 12/13 pathways, which contribute to various processes involved in the regulation of tumor cell biology.…”

Section: Efficacy Of Pepducins In Disease Modelsmentioning

confidence: 99%

Pharmacology, Biodistribution, and Efficacy of GPCR-Based Pepducins in Disease Models

Tressel

Κούκος

Tchernychev

et al. 2010

Methods in Molecular Biology

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G protein-coupled receptors (GPCR) are a superfamily of receptors that are vital in a wide array of physiological processes. Modulation of GPCR signaling has been an intensive area of therapeutic study, mainly due to the diverse pathophysiological significance of GPCRs. Pepducins are cell-penetrating lipidated peptides designed to target the intracellular loops of the GPCR of interest. Pepducins can function as agonists or antagonists of their cognate receptor, making them highly useful compounds for the study of GPCR signaling. Pepducins have been used to control platelet-dependent hemostasis and thrombosis, tumor growth, invasion, and angiogenesis, as well as to improve sepsis outcomes in mice. Pepducins have been successfully designed against a wide variety of GPCRs including the protease-activated receptors (PAR1, 2, 4), the chemokine receptors (CXCR1, 2, 4), the sphingosine-1-phosphate receptor (S1P3), the adrenergic receptor (ADRA1B), and have the potential to help reveal the functions of intractable GPCRs. Pharmacokinetic, pharmacodynamic, and biodistribution studies have showed that pepducins are widely distributed throughout the body except the brain and possess appropriate drug-like properties for use in vivo. Here, we discuss the delivery, pharmacology, and biodistribution of pepducins, as well as the effects of pepducins in models of inflammation, cardiovascular disease, cancer, and angiogenesis.

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“…Functional thrombin receptors have been identified in human pancreatic cancer cells but not in healthy pancreatic tissue. 38 Aside from its procoagulant roles, thrombin enhances the adhesion of pancreatic adenocarcinoma cells to extracellular matrix proteins and to endothelial cells, suggesting that it is important for pancreatic tumour growth and invasion. 7 …”

Section: Introductionmentioning

confidence: 99%

The relationship between pancreatic cancer and hypercoagulability: a comprehensive review on epidemiological and biological issues

et al. 2019

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It has long been recognised that pancreatic cancer induces a hypercoagulable state that may lead to clinically apparent thrombosis. Although the relationship between pancreatic cancer and hypercoagulability is well described, the underlying pathological mechanism(s) and the interplay between these pathways remain a matter of intensive study. This review summarises existing data on epidemiology and pathogenesis of thrombotic complications in pancreatic cancer with a particular emphasis on novel pathophysiological pathways. Pancreatic cancer is characterised by high tumoural expression of tissue factor, activation of leukocytes with the release of neutrophil extracellular traps, the dissemination of tumour-derived microvesicles that promote hypercoagulability and increased platelet activation. Furthermore, other coagulation pathways probably contribute to these processes, such as those that involve heparanase, podoplanin and hypofibrinolysis. In the era in which heparin and its derivatives—the currently recommended therapy for cancer-associated thrombosis—might be superseded by direct oral anticoagulants, novel data from mouse models of cancer-associated thrombosis suggest the possibility of future personalised therapeutic approaches. In this dynamic era for cancer-associated thrombosis, the discovery of novel prothrombotic and proinflammatory mechanisms will potentially uncover pharmacological targets to prevent and treat thrombosis without adversely affecting haemostasis.

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Untitled

Cited by 38 publications

References 33 publications

Identification of genes involved in growth inhibition of breast cancer cells transduced with estrogen receptor

Identification of genes involved in growth inhibition of breast cancer cells transduced with estrogen receptor

Pharmacology, Biodistribution, and Efficacy of GPCR-Based Pepducins in Disease Models

The relationship between pancreatic cancer and hypercoagulability: a comprehensive review on epidemiological and biological issues

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