Osteosarcoma cell‐calcium signaling through tissue factor–factor VIIa complex and factor Xa

Daubie, Valéry; Decker, Robert De; Nicaise, Charles; Pochet, Roland

doi:10.1016/j.febslet.2007.04.078

Cited by 12 publications

(8 citation statements)

References 16 publications

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“…Moreover, it has been shown that FXainduced PAR-1 activation enhances nuclear factor KB activity, as well as expression of angiogenesis-promoting gene, Cyr6l, and connective tissue growth factor (CTGF) in Hela cells (Riewald et al, 2001). Similarly, FXa-induced PAR-1 and -2 activation enhances cell viability by a sustained calcium signaling in human osteosarcoma cells (Daubie et al, 2007). Furthermore, Morris et al (2006) demonstrated that PAR-2 is essential for FXa-induced signaling, migration and invasion of breast cancer cells.…”

Section: Effect Of Fxa In Cancer Pathologymentioning

confidence: 99%

Factor Xa Signaling Contributes to the Pathogenesis of Inflammatory Diseases

Ebrahimi

Rezaei

Seiri

et al. 2016

Journal Cellular Physiology

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The coagulation protease Factor Xa (FXa) triggers a variety of signaling pathways through activation of protease-activated receptors (PARs) and non-PAR receptors. FXa-mediated signaling is strongly implicated in the pathogenesis of several inflammatory diseases including fibrosis, cardiovascular diseases, and cancer. Thus, targeting of FXa can have great clinical significance in terms of the treatment of these disorders. This review summarizes the current knowledge about the mechanism of FXa signaling in cellular and animal systems under (patho) physiological conditions for a better understanding and hence a better management of FXa-induced disorders. J. Cell. Physiol. 232: 1966-1970, 2017. © 2016 Wiley Periodicals, Inc.

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Section: Effect Of Fxa In Cancer Pathologymentioning

confidence: 99%

Factor Xa Signaling Contributes to the Pathogenesis of Inflammatory Diseases

Ebrahimi

Rezaei

Seiri

et al. 2016

Journal Cellular Physiology

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“…However, PAR 2 is now known to be activated by the Tissue Factor/VIIa binary complex and by Factor Xa, which can cleave PAR 2 either independently, or with greater efficiency as part of a ternary complex with TF and VIIa ( Camerer et al , 2000 ; Riewald et al , 2001 ). PAR 2 activation by coagulation proteases is now known to initiate a number of important signalling events, including signalling and migration of cancer cells ( Morris et al , 2006 ), induction of angiogenesis ( Belting et al , 2004 ; Uusitalo‐Jarvinen et al , 2007 ) and signalling in Osteosarcoma cells ( Daubie et al , 2007 ).…”

Section: Searching For the Proteinases Responsible For Par Activationmentioning

confidence: 99%

Proteinases and signalling: pathophysiological and therapeutic implications via PARs and more

Ramachandran

Hollenberg

2008

British J Pharmacology

289

331

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Proteinases like thrombin, trypsin and tissue kallikreins are now known to regulate cell signaling by cleaving and activating a novel family of G‐protein‐coupled proteinase‐activated receptors (PARs 1–4) via exposure of a tethered receptor‐triggering ligand. On their own, short synthetic PAR‐selective PAR‐activating peptides (PAR‐APs) mimicking the tethered ligand sequences can activate PARs 1, 2 and 4 and cause physiological responses both in vitro and in vivo. Using the PAR‐APs as sentinel probes in vivo, it has been found that PAR activation can affect the vascular, renal, respiratory, gastrointestinal, musculoskeletal and nervous systems (both central and peripheral nervous system) and can promote cancer metastasis and invasion. In general, responses triggered by PARs 1, 2 and 4 are in keeping with an innate immune inflammatory response, ranging from vasodilatation to intestinal inflammation, increased cytokine production and increased or decreased nociception. Further, PARs have been implicated in a number of disease states, including cancer and inflammation of the cardiovascular, respiratory, musculoskeletal, gastrointestinal and nervous systems. In addition to activating PARs, proteinases can cause hormone‐like effects by other signalling mechanisms, like growth factor receptor activation, that may be as important as the activation of PARs. We, therefore, propose that the PARs themselves, their activating serine proteinases and their associated signalling pathways can be considered as attractive targets for therapeutic drug development. Thus, proteinases in general must now be considered as ‘hormone‐like’ messengers that can signal either via PARs or other mechanisms. British Journal of Pharmacology (2008) 153, S263–S282; doi:; published online 3 December 2007

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“…In another study, the OS cell line SAOS-2 was shown to express TF, and the TF:FVIIa complex on these cells induced calcium signaling through PAR-2. (19)…”

Section: Introductionmentioning

confidence: 99%

Tissue factor associates with survival and regulates tumour progression in osteosarcoma

Tieken¹,

Verboom²,

Ruf³

et al. 2016

Thromb Haemost

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Osteosarcoma is the most common primary malignant bone tumor. Patients often develop lung metastasis and have a poor prognosis despite extensive chemotherapy and surgical resections. Tissue Factor is associated with poor clinical outcome in a wide range of cancer types, and promotes angiogenesis and metastasis. The role of Tissue Factor in OS tumorigenesis is unknown. 53 osteosarcoma pre-treatment biopsies and four osteosarcoma cell lines were evaluated for Tissue Factor expression, and a possible association with clinical parameters was investigated. Tissue Factor function was inhibited in an osteosarcoma cell line (143B) by shRNA knockdown or specific antibodies, and pro-tumorigenic gene expression, proliferation, matrigel invasion and transwell migration was examined. 143B cells were implanted in mice in the presence of Tissue Factor-blocking antibodies, and tumor volume, micro-vessel density and metastases in the lung were evaluated. Tissue Factor was highly expressed in 73.6% of osteosarcoma biopsies, and expression associated significantly with disease-free survival. Tissue Factor was expressed in all four investigated cell lines. Tissue Factor was knocked down in 143B cells, which led to reduced expression of IL-8, CXCL-1, SNAIL and MMP2, but not MMP9. Tissue Factor knockdown or inhibition with antibodies reduced matrigel invasion. Tissue Factor antibodies limited 143B tumor growth in vivo, and resulted in decreased intra-tumoral micro-vessel density. Furthermore, lung metastasis from the primary tumor was significantly reduced. Thus, Tissue Factor expression in osteosarcoma reduces metastasis-free survival in patients, and increases pro-tumorigenic behavior both in vitro and in vivo.

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Osteosarcoma cell‐calcium signaling through tissue factor–factor VIIa complex and factor Xa

Cited by 12 publications

References 16 publications

Factor Xa Signaling Contributes to the Pathogenesis of Inflammatory Diseases

Factor Xa Signaling Contributes to the Pathogenesis of Inflammatory Diseases

Proteinases and signalling: pathophysiological and therapeutic implications via PARs and more

Tissue factor associates with survival and regulates tumour progression in osteosarcoma

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