Tissue Factor–Factor VII Complex as a Key Regulator of Ovarian Cancer Phenotypes

Koizume, Shiro; Miyagi, Yohei

doi:10.4137/bic.s29318

Cited by 12 publications

(23 citation statements)

References 117 publications

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“…FVII is an enzyme that belongs to the serine protease class [28, 35], whereas FVIII is a protein that is required for the activation of other coagulation factors [36, 37]. The results of the current study showed significant increases in the levels of FVII and FVIII associated with waterpipe and cigarette tobacco smoking.…”

Section: Discussionsupporting

confidence: 57%

Waterpipe Smoking Is Associated with Changes in Fibrinogen, FVII, and FVIII Levels

2018

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Cigarette smoking has been shown to be associated with changes in coagulation factors in the circulation and the subsequent thrombosis development. In this study, the impact of waterpipe smoking on the levels of fibrinogen, factor VII (FVII), and factor VIII (FVIII) was investigated. In addition, the effects of waterpipe smoking were compared to those of cigarette smoking and never smokers. A total of 80 male smokers (40 cigarette smokers and 40 waterpipe smokers) and 40 apparently healthy never smokers were recruited in the study. Both waterpipe smoking and cigarette smoking induced significant increases in the plasma levels of fibrinogen, factor VII, and factor VIII (p < 0.01). The magnitude of the increase in fibrinogen levels induced by waterpipe smoking was higher than that induced by cigarette smoking (p < 0.01), while similar increases were observed in other factors (p > 0.05). In addition, in the waterpipe group, the magnitude of the increase in fibrinogen and factor VIII was higher in the smokers with more than 3 years of use (p < 0.05). In conclusion, similar to cigarette smoking, waterpipe smoking modulates the levels of coagulation factors, suggesting its thrombotic potential.

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Section: Discussionsupporting

confidence: 57%

Waterpipe Smoking Is Associated with Changes in Fibrinogen, FVII, and FVIII Levels

2018

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“…MAPKs (ERK, JNK, and p38), as well as Akt, were reported as the upstream regulators of NF-κB [12,13,14]. Therefore, we would like to investigate the role of these protein kinases in hypoxia-induced TF expression.…”

Section: Resultsmentioning

confidence: 99%

“…To survive and grow in a hypoxic microenvironment, cancer cells must undergo a variety of adaptive changes, including metabolic adaptation, increased resistance to apoptosis, and promotion of angiogenesis and metastasis [10]. In addition, hypoxia-induced upregulation of TF and procoagulant activity has been reported in a variety of cancer types, including, breast cancer [11], ovarian cancer [12], glioma cancer [13], and lung cancer [14]. A major mechanism mediating adaptive responses to hypoxia is the regulation of transcription by hypoxia-inducible factor-1α (HIF-1α) [15].…”

Section: Introductionmentioning

confidence: 99%

YC-1 Prevents Tumor-Associated Tissue Factor Expression and Procoagulant Activity in Hypoxic Conditions by Inhibiting p38/NF-κB Signaling Pathway

Hsieh

Wei

2019

IJMS

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Tissue factor (TF) expressed in cancer cells has been linked to tumor-associated thrombosis, a major cause of mortality in malignancy. Hypoxia is a common feature of solid tumors and can upregulate TF. In this study, the effect of YC-1, a putative inhibitor of hypoxia-inducible factor-1α (HIF-1α), on hypoxia-induced TF expression was investigated in human lung cancer A549 cells. YC-1 selectively prevented hypoxia-induced TF expression and procoagulant activity without affecting the basal TF levels. Surprisingly, knockdown or pharmacological inhibition of HIF-1α failed to mimic YC-1′s effect on TF expression, suggesting other mechanisms are involved. NF-κB, a transcription factor for TF, and its upstream regulator p38, were activated by hypoxia exposure. Treatment of hypoxic A549 cells with YC-1 prevented the activation of both NF-κB and p38. Inhibition of p38 suppressed hypoxia-activated NF-κB, and inhibited TF expression and activity to similar levels as treatment with an NF-κB inhibitor. Furthermore, stimulation of p38 by anisomycin reversed the effects of YC-1. Taken together, our results suggest that YC-1 prevents hypoxia-induced TF in cancer cells by inhibiting the p38/NF-κB pathway, this is distinct from the conventional anticoagulants that systemically inhibit blood coagulation and may shed new light on approaches to treat tumor-associated thrombosis.

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“…Dr. Koizume and Dr. Miyagi highlight the role of secretory protein tissue factor (TF) and associated cellular signaling as a diagnostic biomarker in several types of cancer including ovarian cancer. 9 Oncogenic signaling alterations also endow cells with resistance to anticancer therapy. Dr. Zonathan Schatz’s review on manipulation of increased oncogenic signaling to therapeutic benefit provides an insight for novel therapeutic intervention that can be designed to target cancer-sustaining and altered growth-promoting signaling that evades current therapeutic regimens.…”

Section: Supplement Aims and Scopementioning

confidence: 99%

Signaling Pathways as Biomarkers

Sahasrabuddhe

Rolland

Banerjee³

2015

Biomark�Cancer

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Tissue Factor–Factor VII Complex as a Key Regulator of Ovarian Cancer Phenotypes

Cited by 12 publications

References 117 publications

Waterpipe Smoking Is Associated with Changes in Fibrinogen, FVII, and FVIII Levels

Waterpipe Smoking Is Associated with Changes in Fibrinogen, FVII, and FVIII Levels

YC-1 Prevents Tumor-Associated Tissue Factor Expression and Procoagulant Activity in Hypoxic Conditions by Inhibiting p38/NF-κB Signaling Pathway

Signaling Pathways as Biomarkers

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