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http://purl.uniprot.org/citations/21543928http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/21543928http://www.w3.org/2000/01/rdf-schema#comment"

Objective

Tumor-associated macrophage infiltration and up-regulation of tissue factor-factor VII (TF-FVIIa) complex have been observed in the peritoneum and stroma of epithelial ovarian cancer (EOC). However, it is not clear how tumor-associated macrophage and TF-FVIIa complex promotes EOC invasion. In the present study, we aimed to determine the mechanism by which interaction of TF-FVIIa and monocytes (MOs) promotes EOC metastasis.

Method

Matrigel invasion assay was used to analyze the potential of EOC metastasis. Enzyme-linked immunosorbent assay and real-time polymerase chain reaction were used to detect expressions of cytokines and chemokines. Fluorescence-activated cell sorting was used to count the percentage of CD14, CD68, and CD163 of MOs.

Results

We found that the TF-FVIIa complex caused dynamic changes in MOs cytokine and chemokine expression. CD14 and CD163 were also upregulated on MOs by TF-FVIIa. Epithelial ovarian cancer cells were cocultured with TF-FVIIa-stimulated MOs, demonstrating increased invasion potential. Interleukin 8 (IL-8) was proposed as the major chemoattractant mediating EOC invasion based on MOs messenger RNA and protein expression profiles. Anti-IL-8 monoclonal neutralizing antibody attenuated EOC cell invasion in a concentration-dependent manner, and tumor necrosis factor α from TF-FVIIa-stimulated MOs was observed to amplify IL-8 production. The following transcription factors in MOs were activated by TF-FVIIa and inhibited by the tissue factor pathway inhibitor: oncogenes HIF-1α, HIF-1β, Oct I, Oct II, and Egr-1; inflammatory mediators c-Fos and c-Rel; and STAT family members STAT5A and STAT5B.

Conclusions

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."xsd:string
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http://purl.uniprot.org/citations/21543928http://purl.uniprot.org/core/author"Cheng Z."xsd:string
http://purl.uniprot.org/citations/21543928http://purl.uniprot.org/core/author"Ma Z."xsd:string
http://purl.uniprot.org/citations/21543928http://purl.uniprot.org/core/author"Li W."xsd:string
http://purl.uniprot.org/citations/21543928http://purl.uniprot.org/core/author"Wang Y."xsd:string
http://purl.uniprot.org/citations/21543928http://purl.uniprot.org/core/author"Xu H."xsd:string
http://purl.uniprot.org/citations/21543928http://purl.uniprot.org/core/author"Zhang T."xsd:string
http://purl.uniprot.org/citations/21543928http://purl.uniprot.org/core/author"Wang X."xsd:string
http://purl.uniprot.org/citations/21543928http://purl.uniprot.org/core/author"Wang R."xsd:string
http://purl.uniprot.org/citations/21543928http://purl.uniprot.org/core/date"2011"xsd:gYear
http://purl.uniprot.org/citations/21543928http://purl.uniprot.org/core/name"Int J Gynecol Cancer"xsd:string
http://purl.uniprot.org/citations/21543928http://purl.uniprot.org/core/pages"616-624"xsd:string
http://purl.uniprot.org/citations/21543928http://purl.uniprot.org/core/title"Tissue factor-factor VIIa complex induces epithelial ovarian cancer cell invasion and metastasis through a monocytes-dependent mechanism."xsd:string
http://purl.uniprot.org/citations/21543928http://purl.uniprot.org/core/volume"21"xsd:string
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