دورية أكاديمية
أعرض في EDS

Epithelial ovarian cancer-induced angiogenic phenotype of human omental microvascular endothelial cells may occur independently of VEGF signaling.

التفاصيل البيبلوغرافية
العنوان: Epithelial ovarian cancer-induced angiogenic phenotype of human omental microvascular endothelial cells may occur independently of VEGF signaling.
المؤلفون: Winiarski BK; Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, Devon, United Kingdom., Wolanska KI; Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, Devon, United Kingdom., Rai S; Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, Devon, United Kingdom., Ahmed T; Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, Devon, United Kingdom., Acheson N; Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, Devon, United Kingdom ; Royal Devon and Exeter NHS Foundation Trust, Exeter, United Kingdom., Gutowski NJ; Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, Devon, United Kingdom ; Royal Devon and Exeter NHS Foundation Trust, Exeter, United Kingdom., Whatmore JL; Institute of Biomedical and Clinical Science, University of Exeter Medical School, Exeter, Devon, United Kingdom.
المصدر: Translational oncology [Transl Oncol] 2013 Dec 01; Vol. 6 (6), pp. 703-14. Date of Electronic Publication: 2013 Dec 01 (Print Publication: 2013).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Neoplasia Press Country of Publication: United States NLM ID: 101472619 Publication Model: eCollection Cited Medium: Print ISSN: 1936-5233 (Print) Linking ISSN: 19365233 NLM ISO Abbreviation: Transl Oncol Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: [Ann Arbor, MI] : Neoplasia Press
مستخلص: Epithelial ovarian cancer (EOC) metastasizes transcoelomically to the peritoneum and omentum, and despite surgery and chemotherapy, recurrent disease is likely. Metastasis requires the induction of proangiogenic changes in the omental microenvironment and EOC-induced omental angiogenesis is currently a key therapeutic target. In particular, antiangiogenic therapies targeting the vascular endothelial growth factor A (VEGFA) pathway are commonly used, although, with limited effects. Here, using human omental microvascular endothelial cells (HOMECs) and ovarian cancer cell lines as an in vitro model, we show that factors secreted from EOC cells increased proliferation, migration, and tube-like structure formation in HOMECs. However, EOC-induced angiogenic tube-like formation and migration were unaffected by inhibition of tyrosine kinase activity of VEGF receptors 1 and 2 (Semaxanib; SU5416) or neutralization of VEGFA (neutralizing anti-VEGFA antibody), although VEGFA165-induced HOMEC migration and tube-like structure formation were abolished. Proteomic investigation of the EOC secretome identified several alternative angiogenesis-related proteins. We screened these for their ability to induce an angiogenic phenotype in HOMECs, i.e., proliferation, migration, and tube-like structure formation. Hepatocyte growth factor (HGF) and insulin-like growth factor binding protein 7 (IGFBP-7) increased all three parameters, and cathepsin L (CL) increased migration and tubule formation. Further investigation confirmed expression of the HGF receptor c-Met in HOMECs. HGF- and EOC-induced proliferation and angiogenic tube structure formation were blocked by the c-Met inhibitor PF04217903. Our results highlight key alternative angiogenic mediators for metastatic EOC, namely, HGF, CL, and IGFBP-7, suggesting that effective antiangiogenic therapeutic strategies for this disease require inhibition of multiple angiogenic pathways.
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تواريخ الأحداث: Date Created: 20140128 Date Completed: 20140127 Latest Revision: 20211021
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC3890705
DOI: 10.1593/tlo.13529
PMID: 24466373
قاعدة البيانات: MEDLINE
الوصف
تدمد:1936-5233
DOI:10.1593/tlo.13529