Up-regulation of VEGF-C secreted by cancer cells and not VEGF-A correlates with clinical evaluation of lymph node metastasis in esophageal squamous cell carcinoma (ESCC)

Krzystek−Korpacka, Małgorzata; Matusiewicz, Małgorzata; Diakowska, Dorota; Grabowski, Krzysztof; Blachut, Katarzyna; Banaś, Teresa

doi:10.1016/j.canlet.2006.08.011

Cited by 49 publications

(42 citation statements)

References 30 publications

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“…In situations, where the VEGF-A/ VEGF-C balance in the tumour microenvironment is shifted in favour of VEGF-C, the VEGF-C-mediated responses would likely dominate. For example, higher serum concentrations of VEGF-C than that of VEGF-A, believed to be tumour derived, correlates with lymph node metastasis in patients with squamous cell carcinoma of the oesophagus (Krzystek-Korpacka et al, 2007). The rate of secretion of VEGF-C in vitro by the highly metastatic human breast cancer cell line MDA-MB-231 was found to be 10 times than that of VEGF-A (Timoshenko et al, 2006).…”

Section: Discussionmentioning

confidence: 96%

Migration-promoting role of VEGF-C and VEGF-C binding receptors in human breast cancer cells

2007

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Vascular endothelial growth factor C (VEGF-C) is a lymphangiogenic factor over-expressed in highly metastatic, cyclooxygenase (COX)-2 expressing breast cancer cells. We tested the hypothesis that tumour-derived VEGF-C may play an autocrine role in metastasis by promoting cellular motility through one or more VEGF-C-binding receptors VEGFR-2, VEGFR-3, neuropilin (NRP)-1, NRP-2, and integrin α 9 β 1. We investigated the expression of these receptors in several breast cancer cell lines (MDA-MB-231, Hs578T, SK-BR-3, T-47D, and MCF7) and their possible requirement in migration of two VEGF-C-secreting, highly metastatic lines MDA-MB-231 and Hs578T. While cell lines varied significantly in their expression of above VEGF-C receptors, migratory activity of MDA-MB-231 and Hs578T cells was linked to one or more of these receptors. Depletion of endogenous VEGF-C by treatments with a neutralising antibody, VEGF-C siRNA or inhibitors of Src, EGFR/Her2/neu and p38 MAP kinases which inhibited VEGF-C production, inhibited cellular migration, indicating the requirement of VEGF-C for migratory function. Migration was differentially attenuated by blocking or downregulation of different VEGF-C receptors, for example treatment with a VEGFR-2 tyrosine kinase inhibitor, NRP-1 and NRP-2 siRNA or α 9 β 1 integrin antibody, indicating the participation of one or more of the receptors in cell motility. This novel role of tumour-derived VEGF-C indicates that breast cancer metastasis can be promoted by coordinated stimulation of lymphangiogenesis and enhanced migratory activity of breast cancer cells.

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Section: Discussionmentioning

confidence: 96%

Migration-promoting role of VEGF-C and VEGF-C binding receptors in human breast cancer cells

2007

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“…VEGF expression has been correlated with poor prognosis in many cancers, including carcinomas of the breast, kidney, colon, brain, ovary, cervix, thyroid, bladder, esophagus, and prostate, and in osteoid and soft tissue sarcomas and pediatric tumors (Liu et al, 1995). Significantly elevated levels of sVEGF have also been reported in esophageal (Krzystek-Korpacka et al, 2007;Kimura et al, 2008) and gastric cancer patients (Wang et al, 2007;Seo et al, 2010) than healthy controls. The measurement of the circulating soluble marker of angiogenesis has more advantages over other subjective approaches like immunohistochemical assessments or immunoassays.…”

Section: Discussionmentioning

confidence: 99%

Association of −2549 Insertion/Deletion Polymorphism of Vascular Endothelial Growth Factor with Breast Cancer in North Indian Patients

Kapahi

Manjari²,

Uppal³

et al. 2013

Genetic Testing and Molecular Biomarkers

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“…Tumor expression of lymphangiogenic factors, specifically vascular endothelial growth factor-C (VEGF-C) and VEGF-D, has been correlated with lymphatic metastasis both in humans and in animal models (3)(4)(5)(6). For example, one report showed serum VEGF-C levels in patients with squamous cell carcinoma of the esophagus to be on the order of 16 to 22 ng/mL, compared with 11 ng/mL for healthy patients (7). Because the expression of the primary receptor of VEGF-C and VEGF-D, VEGF receptor-3 (VEGFR-3), is largely restricted to lymphatic endothelial cells (LEC; ref.…”

Section: Introductionmentioning

confidence: 99%

Vascular Endothelial Growth Factor-C and C-C Chemokine Receptor 7 in Tumor Cell–Lymphatic Cross-talk Promote Invasive Phenotype

et al. 2008

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Up-regulation of VEGF-C secreted by cancer cells and not VEGF-A correlates with clinical evaluation of lymph node metastasis in esophageal squamous cell carcinoma (ESCC)

Cited by 49 publications

References 30 publications

Migration-promoting role of VEGF-C and VEGF-C binding receptors in human breast cancer cells

Migration-promoting role of VEGF-C and VEGF-C binding receptors in human breast cancer cells

Association of −2549 Insertion/Deletion Polymorphism of Vascular Endothelial Growth Factor with Breast Cancer in North Indian Patients

Vascular Endothelial Growth Factor-C and C-C Chemokine Receptor 7 in Tumor Cell–Lymphatic Cross-talk Promote Invasive Phenotype

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