Tissue factor expression in human colorectal carcinoma

Seto, Shiro; Onodera, Hisashi; Kaido, Toshimi; Yoshikawa, Akira; Ishigami, Shunichi; Arii, Shigeki; Imamura, Masayuki

doi:10.1002/(sici)1097-0142(20000115)88:2<295::aid-cncr8>3.0.co;2-u

Cited by 157 publications

(35 citation statements)

References 17 publications

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“…The signal transduction pathways involved in antiapoptosis include the PI3 kinase/ PKB and the p42/p44 MAP kinase pathways. Importantly, the interaction of TF has previously been shown to result in the stimulation of both PI3 kinase-and p42/ p44 MAP kinase-dependent signaling (Poulsen et al, 1998;Camerer et al, 1999;Versteeg et al, 2000Versteeg et al, , 2002, whereas the TF overexpression is associated with successful metastasis (Mueller et al, 1992;Shigemori et al, 1998;Seto et al, 2000). Therefore, we investigated the potential of TF overexpression to confer cell survival and inhibition of apoptosis, especially in the context of loss-of-adhesion-induced cell death.…”

Section: Discussionmentioning

confidence: 93%

“…Tumor cells and metastatic cells often overexpress TF levels (Mueller et al, 1992;Shigemori et al, 1998;Seto et al, 2000), but FVII levels, normally reaching plasma levels of 10 nM, do not allow for much variation. Therefore, it is not likely that enhanced levels of FVII contribute to survival signaling in blood-borne tumor cells.…”

Section: Discussionmentioning

confidence: 99%

“…The primary initiator of coagulation, TF, is frequently upregulated on the surface of tumor cells and metastatic cells (Hamada et al, 1996;Vrana et al, 1996;Shigemori et al, 1998;Seto et al, 2000;Ueda et al, 2001). Complexation of TF with its natural ligand FVIIa leads to the activation of PKB, also known as c-Akt (Versteeg et al, 2000(Versteeg et al, , 2002 in several cell types.…”

Section: Fviia Inhibits Apoptosis Induced By Serum Deprivationmentioning

confidence: 99%

“…The overexpression of TF, up to a 1000-fold increase over normal levels, is a striking feature of metastatic cells upon comparison with nonmetastatic cells (Mueller et al, 1992). Moreover, TF expression showed to be a significant and independent risk factor for hepatic metastasis in patients with colorectal cancer (Shigemori et al, 1998;Seto et al, 2000). In experimental models, the introduction of melanoma cells that overexpress TF in severe combined immunodeficient mice promotes efficient hematogeneous metastasis (Mueller et al, 1992).…”

Section: Introductionmentioning

confidence: 98%

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Coagulation factors VIIa and Xa inhibit apoptosis and anoikis

et al. 2004

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The molecular mechanisms enabling cancer cells to survive loss-of-adhesion-induced apoptosis in the early phases of metastasis remain largely obscure. Interestingly, the overexpression of tissue factor (TF) on tumor cells is associated with successful metastasis and it has now become clear that coagulation factor VIIa (FVIIa), the natural binding partner of TF induces signal transduction in TF-expressing cells. Hence, we investigated the effects of FVIIa-TF interaction on cell survival. We observed that FVIIa, at physiologically relevant concentrations, inhibits cell death and caspase-3 activation induced by serum deprivation and loss of adhesion (lack of integrin signaling) in TF-overexpressing cells, but not in non-TFexpressing cells. This FVIIa effect was not dependent on the formation of the downstream coagulation products FXa or thrombin and was inhibited using an active siteblocked form of FVIIa (FVIIai). FVIIa incubation resulted in the prolonged activation of both the phosphatidylinositide-3-(OH) kinase and p42/p44 MAP kinase pathways, and studies employing pharmacological inhibitors revealed that both the pathways are required for FVIIa-induced cell survival and inhibition of caspase-3 activity. Finally, TF:FVIIa-induced FXa generation dramatically increased cell survival. We propose that FVIIa-induced cell survival may explain why overexpression of TF is associated with successful metastasis.

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Fviia Inhibits Apoptosis Induced By Serum Deprivationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

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Coagulation factors VIIa and Xa inhibit apoptosis and anoikis

et al. 2004

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“…High levels of TF have been reported in a variety of tumor cells; metastatic human melanoma cells have, for example, been shown to express a 1000-fold higher level of TF than their non-metastatic counterparts (6). The expression of TF correlates with the potential for metastasis (53)(54)(55) and angiogenesis (26), and the proteolytic activity of FVIIa is crucial in TF-dependent metastasis (5, 7). Here we have shown that up-regulation of the synthesis of IL-8 protein depends on the proteolytic activity of the TF-FVIIa complex.…”

Section: Discussionmentioning

confidence: 99%

Factor VIIa Induces Tissue Factor-dependent Up-regulation of Interleukin-8 in a Human Keratinocyte Line

Wang¹,

Gjernes

Prydz

2002

Journal of Biological Chemistry

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Tissue factor (TF), a transmembrane receptor for the serine protease coagulation factor VII(a) (FVIIa), is the main initiator of the coagulation cascade. Through incompletely elucidated mechanisms, TF serves additional functions in tumor-associated angiogenesis and metastasis. We have studied interleukin-8 (IL-8) as a possible link between TF-FVIIa complex formation and subsequent processes. Recombinant human FVIIa induced the up-regulation of both IL-8 mRNA and protein in a FVIIa dose-and time-dependent fashion. A neutralizing antibody to TF reduced this induction by 93 ؎ 5%. Active site-inhibited FVIIa had no stimulatory effect and completely blocked that of FVIIa. This confirms that the increased IL-8 production was dependent on the formation of TF-FVIIa complexes and the proteolytic activity of FVIIa. The IL-8 promoter contains DNA binding sites for nuclear factor-B (NF-B) and activator protein-1 (AP-1). In response to FVIIa, the DNA binding activity of both NF-B and AP-1 was enhanced in an electrophoretic mobility shift assay. In addition, the IL-8 promoter was transcriptionally activated both in a luciferase reporter system and a nuclear run-off assay. Moreover, IL-8 mRNA stability was significantly enhanced by FVIIa-induced activation of the mitogen-activated protein kinases ERK1/2 and p38. Taken together, TF-FVIIa signaling induced increased transcription as well as mRNA stabilization leading to the significant up-regulation of IL-8 protein synthesis.

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