Tissue Factor-Factor VIIa Complex Induces Epithelial Ovarian Cancer Cell Invasion and Metastasis Through a Monocytes-Dependent Mechanism

Zhang, Ting; Wang, Ruili; Cheng, Zhongping; Xu, Hong; Li, Weiping; Wang, Ying

doi:10.1097/igc.0b013e3182150e98

Cited by 23 publications

(20 citation statements)

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“…have proposed that tumor cells might be activated by the macrophages and secrete angiogenic factors in head‐and‐neck squamous cell carcinomas . Our previous studies have certified TNF‐α expression upstream of IL‐8 expression in macrophage, when we added TNF‐α blocking antibody, IL‐8 expression was decreased . It has been reported that indirect interactions between tumor and stroma cells enhance the expression of angiogenic factors, such as IL‐1, and TNF‐α, in a conditioned medium, can increase IL‐8 expression.…”

Section: Discussionmentioning

confidence: 80%

“…Interleukin‐13 (IL‐13) and IL‐4 can induce the differentiation of macrophages into M2 cells, with IL‐10 high and IL‐12 low phenotype. Our previous study have reported that coagulation factors II, III and XII induce the differentiation of peripheral blood monocytes from healthy women into M2‐like macrophages, and participate in promoting EOC progression . In our previous study, we have demonstrated that CD68 + macrophages are in close contact with CD31 + endothelial cells in peritoneum in the presence of EOC.…”

mentioning

confidence: 87%

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Interaction of monocytes/macrophages with ovarian cancer cells promotes angiogenesis in vitro

et al. 2013

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It has been established that macrophages and endothelial cells infiltrate peritoneum in the vicinity of tumor implants of epithelial ovarian cancer (EOC). This study investigates whether the interaction of ovarian cancer cells and tumor-associated macrophages could promote the involvement of endothelial cells in angiogenesis. Macrophage phenotypes were detected by fluorescence-activated cell sorting, and cytokine/chemokine secretion was measured by enzyme linked immunosorbent assay. The effect of co-culture of ovarian cancer cells and tumor-associated macrophage (TAM) cells on endothelial cell migration and tube formation was investigated. Signaling pathway mediators were also evaluated for their potential roles in endothelial cell activation by ovarian cancer cells co-cultured with TAM cells. Our results showed that higher expression of interleukin-8 (IL-8) expression associated with 54.26 ± 34.46% of TAM infiltration of peritoneum was significantly higher than 16.58 ± 17.74% of CD3 + T-cell by immunofluorescence co-staining and confocal microscopy. THP-1 cells exhibited M2-polarized phenotype markers with high proportion of CD68 + , CD206+ and CD204 + markers after phorbol 12-myristate 13-acetate (PMA) treatment, After co-culturing with TAM cells in a transwell chamber system, EOC cells (SKOV3) increased their IL-8 expression at the level of mRNA and protein. After exposure to the conditioned medium obtained by co-culturing TAM and SKOV3 cells, the migration and tube formation of endothelial cells were enhanced significantly. Furthermore, the upregulation of IL-8 expression in ovarian cancer cells induced by macrophages could be inhibited by pyrollidine dithiocarbamate, an inhibitor of nuclear factor (NF)-jB signal pathway. We suggest that the interaction of ovarian cancer cells and tumor-associated macrophages enhances the ability of endothelial cells to promote the progression of ovarian cancer. (Cancer Sci 2013; 104: 516-523) E pithelial ovarian cancer (EOC) accounts for 90% of all ovarian cancers and has become the leading cause of death from gynecological cancers in North America and Europe.(1)A remarkable feature of advanced EOC is the presence of widespread peritoneal metastases at the time of the initial diagnosis. However, the mechanisms of peritoneal seeding, spreading and progression remain elusive.Tumor microenvironment consists of various stromal cells, including activated endothelial cells, tumor-associated macrophages (TAMs), fibroblasts, and bone marrow-derived cells.(2)Our previous study has confirmed that more than 75% of mononuclear immune cells in peritoneum close to a tumor implant were TAM, which mimic chronic inflammation. Most studies reported that infiltrating TAMs were associated with cancer progression.(4-7) Tumor-associated macrophages might be recruited from peripheral blood by chemokines and then positioned in the tumor stroma. Those macrophages could be 'educated' and differentiated into M1 or M2 forms as a result of activation by some molecular factors. Interferon-c (IFN-c)

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Section: Discussionmentioning

confidence: 80%

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confidence: 87%

Interaction of monocytes/macrophages with ovarian cancer cells promotes angiogenesis in vitro

et al. 2013

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“…CTCs accompany metastatic disease across all major types of carcinomas (Allard et al, 2004). Tumors have been shown to express TF in vivo , and TF expression has been shown to correlate with metastatic potential (Zacharski et al, 1983, 1986; Lee et al, 2011; Liu et al, 2011; Ma et al, 2011; Tian et al, 2011; Xu et al, 2011; Gil-Bernabe et al, 2012). Therefore, the process of hematogenous metastasis may present TF-expressing tumor cells to blood in the absence of a blood vessel injury.…”

Section: Ctc–blood Protein Interactionsmentioning

confidence: 99%

Do circulating tumor cells play a role in coagulation and thrombosis?

Tormoen¹,

Haley²,

Levine³

et al. 2012

Front. Oncol.

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Cancer induces a hypercoagulable state, and patients with cancer who suffer a thrombotic event have a worse prognosis than those who do not. Recurrent pathologic thrombi in patients with cancer are clinically managed with anticoagulant medications; however, anticoagulant prophylaxis is not routinely prescribed owing to a complex variety of patient and diagnosis related factors. Early identification of patients at risk for cancer-associated thrombosis would allow for personalization of anticoagulant prophylaxis and likely reduce morbidity and mortality for many cancers. The environment in which a thrombosis develops in a patient with cancer is complex and unique from patients without cancer, which creates therapeutic challenges but may also provide targets for the development of clinical assays in this context. Circulating tumor cells (CTCs) may play a role in the association between cancer and thrombosis. Cancer metastasis, the leading cause of cancer-related deaths, is facilitated by the hematogenous spread of CTCs, and CTCs accompany metastatic disease across all major types of carcinomas. The role of CTCs in the pathogenesis of thrombosis has not been studied due to the previous difficulty in identifying these rare cells, but the interaction between these circulating cells and the coagulation system is an area of study that demands attention. The development of CTC detection platforms presents a new tool by which to characterize the role for CTCs in cancer-related hypercoagulability. In addition, this area of study presents a new avenue for assessing the risk of cancer-associated thrombosis and represents a potential tool for predicting which patients may benefit from anticoagulant prophylaxis. In this review, we will discuss the evidence in support of CTC induced hypercoagulability, and highlight areas where CTC-detection platforms may provide prognostic insight into the risk of developing thrombosis for patients with cancer.

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“…A database search revealed that PAR1 transcript levels are significantly higher in EOC tissues compared with those in normal ovarian tissues [37]. In addition, immune cells treated with TF-fVIIa complex potentially included in ascites can augment secretion of cytokines such as interleukin (IL)-8 (CXCL8), thereby increasing the motility and invasiveness of EOC cells [38]. EOC cells can secrete extracellular vesicles (EVs) associated with high levels of TF or TF-fVIIa associated with procoagulant activity, potentially leading to venous thromboembolism (VTE) [28,29,39].…”

Section: Potential Relationship Between Blood Coagulation and Inflmentioning

confidence: 99%

Potential Coagulation Factor-Driven Pro-Inflammatory Responses in Ovarian Cancer Tissues Associated with Insufficient O2 and Plasma Supply

Koizume¹,

Miyagi²

2017

IJMS

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Tissue factor (TF) is a cell surface receptor for coagulation factor VII (fVII). The TF-activated fVII (fVIIa) complex is an essential initiator of the extrinsic blood coagulation process. Interactions between cancer cells and immune cells via coagulation factors and adhesion molecules can promote progression of cancer, including epithelial ovarian cancer (EOC). This process is not necessarily advantageous, as tumor tissues generally undergo hypoxia due to aberrant vasculature, followed by reduced access to plasma components such as coagulation factors. However, hypoxia can activate TF expression. Expression of fVII, intercellular adhesion molecule-1 (ICAM-1), and multiple pro-inflammatory cytokines can be synergistically induced in EOC cells in response to hypoxia along with serum deprivation. Thus, pro-inflammatory responses associated with the TF-fVIIa–ICAM-1 interaction are expected within hypoxic tissues. Tumor tissue consists of multiple components such as stromal cells, interstitial fluid, albumin, and other micro-factors such as proton and metal ions. These factors, together with metabolism reprogramming in response to hypoxia and followed by functional modification of TF, may contribute to coagulation factor-driven inflammatory responses in EOC tissues. The aim of this review was to describe potential coagulation factor-driven inflammatory responses in hypoxic EOC tissues. Arguments were extended to clinical issues targeting this characteristic tumor environment.

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Tissue Factor-Factor VIIa Complex Induces Epithelial Ovarian Cancer Cell Invasion and Metastasis Through a Monocytes-Dependent Mechanism

Abstract: Our study suggested that the interaction between the TF-FVIIa complex might play a role in mediating EOC invasion and metastasis depending on MOs mechanism.

Cited by 23 publications

References 20 publications

Interaction of monocytes/macrophages with ovarian cancer cells promotes angiogenesis in vitro

Interaction of monocytes/macrophages with ovarian cancer cells promotes angiogenesis in vitro

Do circulating tumor cells play a role in coagulation and thrombosis?

Potential Coagulation Factor-Driven Pro-Inflammatory Responses in Ovarian Cancer Tissues Associated with Insufficient O2 and Plasma Supply

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