BACKGROUND: Vascular endothelial growth factor C (VEGF-C) stimulates tumor lymphangiogenesis (i.e., formation of lymphatic vessels) and metastasis to regional lymph nodes by interacting with VEGF receptor 3 (VEGFR-3). We sought to determine whether inhibiting VEGFR-3 signaling, and thus tumor lymphangiogenesis, would inhibit tumor metastasis. METHODS: We used the highly metastatic human lung cancer cell line NCI-H460-LNM35 (LNM35) and its parental line NCI-H460-N15 (N15) with low metastatic capacity. We inserted genes by transfection and established a stable N15 cell line secreting VEGF-C and a LNM35 cell line secreting the soluble fusion protein VEGF receptor 3-immunoglobulin (VEGFR-3-Ig, which binds VEGF-C and inhibits VEGFR-3 signaling). Control lines were transfected with mock vectors. Tumor cells were implanted subcutaneously into severe combined immunodeficient mice (n = 6 in each group), and tumors and metastases were examined 6 weeks later. In another approach, recombinant aden
%0 Journal Article
%1 He.2002
%A He, Y.
%A Kozaki, K.
%A Karpanen, T.
%A Koshikawa, K.
%A Yla-Herttuala, S.
%A Takahashi, T.
%A Alitalo, K.
%D 2002
%J J.Natl.Cancer Inst.
%K & Animals Antibodies Blotting C Cell Cells Cultured D Division Endothelial Expression Factor Factors Female Gene Growth Human Humans Kinase Kinases Laboratories Line Lung Lymph Lymphangiogenesis Lymphatic Metastasis Mice Neoplasm Neoplasms Neoplastic Nodes Protein-Tyrosine RNA Receptor Receptor-3 Receptors Regulation Research Scid Signal Time Transduction Transfection Transplantation Tumor Vascular Vessels Western antagonists blood cells control genetics immunology inhibitors metabolism methods pathology prevention protein secondary supply
%N 11
%P 819-825
%T Suppression of tumor lymphangiogenesis and lymph node metastasis by blocking vascular endothelial growth factor receptor 3 signaling
%U PM:12048269
%V 94
%X BACKGROUND: Vascular endothelial growth factor C (VEGF-C) stimulates tumor lymphangiogenesis (i.e., formation of lymphatic vessels) and metastasis to regional lymph nodes by interacting with VEGF receptor 3 (VEGFR-3). We sought to determine whether inhibiting VEGFR-3 signaling, and thus tumor lymphangiogenesis, would inhibit tumor metastasis. METHODS: We used the highly metastatic human lung cancer cell line NCI-H460-LNM35 (LNM35) and its parental line NCI-H460-N15 (N15) with low metastatic capacity. We inserted genes by transfection and established a stable N15 cell line secreting VEGF-C and a LNM35 cell line secreting the soluble fusion protein VEGF receptor 3-immunoglobulin (VEGFR-3-Ig, which binds VEGF-C and inhibits VEGFR-3 signaling). Control lines were transfected with mock vectors. Tumor cells were implanted subcutaneously into severe combined immunodeficient mice (n = 6 in each group), and tumors and metastases were examined 6 weeks later. In another approach, recombinant aden
@article{He.2002,
abstract = {BACKGROUND: Vascular endothelial growth factor C (VEGF-C) stimulates tumor lymphangiogenesis (i.e., formation of lymphatic vessels) and metastasis to regional lymph nodes by interacting with VEGF receptor 3 (VEGFR-3). We sought to determine whether inhibiting VEGFR-3 signaling, and thus tumor lymphangiogenesis, would inhibit tumor metastasis. METHODS: We used the highly metastatic human lung cancer cell line NCI-H460-LNM35 (LNM35) and its parental line NCI-H460-N15 (N15) with low metastatic capacity. We inserted genes by transfection and established a stable N15 cell line secreting VEGF-C and a LNM35 cell line secreting the soluble fusion protein VEGF receptor 3-immunoglobulin (VEGFR-3-Ig, which binds VEGF-C and inhibits VEGFR-3 signaling). Control lines were transfected with mock vectors. Tumor cells were implanted subcutaneously into severe combined immunodeficient mice (n = 6 in each group), and tumors and metastases were examined 6 weeks later. In another approach, recombinant aden},
added-at = {2010-02-05T11:28:39.000+0100},
author = {He, Y. and Kozaki, K. and Karpanen, T. and Koshikawa, K. and Yla-Herttuala, S. and Takahashi, T. and Alitalo, K.},
biburl = {https://www.bibsonomy.org/bibtex/2058093fbd306ed90ab831b5958d7b0aa/kanefendt},
interhash = {68e46439e1fbf3260cc500b417c929ef},
intrahash = {058093fbd306ed90ab831b5958d7b0aa},
journal = {J.Natl.Cancer Inst.},
keywords = {& Animals Antibodies Blotting C Cell Cells Cultured D Division Endothelial Expression Factor Factors Female Gene Growth Human Humans Kinase Kinases Laboratories Line Lung Lymph Lymphangiogenesis Lymphatic Metastasis Mice Neoplasm Neoplasms Neoplastic Nodes Protein-Tyrosine RNA Receptor Receptor-3 Receptors Regulation Research Scid Signal Time Transduction Transfection Transplantation Tumor Vascular Vessels Western antagonists blood cells control genetics immunology inhibitors metabolism methods pathology prevention protein secondary supply},
number = 11,
pages = {819-825},
timestamp = {2010-02-05T11:28:39.000+0100},
title = {Suppression of tumor lymphangiogenesis and lymph node metastasis by blocking vascular endothelial growth factor receptor 3 signaling},
url = {PM:12048269},
volume = 94,
year = 2002
}