Soluble vascular endothelial growth factor receptor-3 suppresses lymphangiogenesis and lymphatic metastasis in bladder cancer View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2011-04-11

AUTHORS

Hanseul Yang, Chan Kim, Min-Ju Kim, Reto A Schwendener, Kari Alitalo, Warren Heston, Injune Kim, Wun-Jae Kim, Gou Young Koh

ABSTRACT

BackgroundMost bladder cancer patients experience lymphatic metastasis in the course of disease progression, yet the relationship between lymphangiogenesis and lymphatic metastasis is not well known. The aim of this study is to elucidate underlying mechanisms of how expanded lymphatic vessels and tumor microenvironment interacts each other and to find effective therapeutic options to inhibit lymphatic metastasis.ResultsThe orthotopic urinary bladder cancer (OUBC) model was generated by intravesical injection of MBT-2 cell lines. We investigated the angiogenesis, lymphangiogenesis, and CD11b+/CD68+ tumor-associated macrophages (TAM) by using immunofluorescence staining. OUBC displayed a profound lymphangiogenesis and massive infiltration of TAM in primary tumor and lymphatic metastasis in lymph nodes. TAM flocked near lymphatic vessels and express higher levels of VEGF-C/D than CD11b- cells. Because VEGFR-3 was highly expressed in lymphatic vascular endothelial cells, TAM could assist lymphangiogenesis by paracrine manner in bladder tumor. VEGFR-3 expressing adenovirus was administered to block VEGF-C/D signaling pathway and clodronate liposome was used to deplete TAM. The blockade of VEGF-C/D with soluble VEGF receptor-3 markedly inhibited lymphangiogenesis and lymphatic metastasis in OUBC. In addition, the depletion of TAM with clodronate liposome exerted similar effects on OUBC.ConclusionVEGF-C/D are the main factors of lymphangiogenesis and lymphatic metastasis in bladder cancer. Moreover, TAM plays an important role in these processes by producing VEGF-C/D. The inhibition of lymphangiogenesis could provide another therapeutic target to inhibit lymphatic metastasis and recurrence in patients with invasive bladder cancer. More... »

PAGES

36

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/1476-4598-10-36

DOI

http://dx.doi.org/10.1186/1476-4598-10-36

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1025341208

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/21481239


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38 schema:description BackgroundMost bladder cancer patients experience lymphatic metastasis in the course of disease progression, yet the relationship between lymphangiogenesis and lymphatic metastasis is not well known. The aim of this study is to elucidate underlying mechanisms of how expanded lymphatic vessels and tumor microenvironment interacts each other and to find effective therapeutic options to inhibit lymphatic metastasis.ResultsThe orthotopic urinary bladder cancer (OUBC) model was generated by intravesical injection of MBT-2 cell lines. We investigated the angiogenesis, lymphangiogenesis, and CD11b+/CD68+ tumor-associated macrophages (TAM) by using immunofluorescence staining. OUBC displayed a profound lymphangiogenesis and massive infiltration of TAM in primary tumor and lymphatic metastasis in lymph nodes. TAM flocked near lymphatic vessels and express higher levels of VEGF-C/D than CD11b- cells. Because VEGFR-3 was highly expressed in lymphatic vascular endothelial cells, TAM could assist lymphangiogenesis by paracrine manner in bladder tumor. VEGFR-3 expressing adenovirus was administered to block VEGF-C/D signaling pathway and clodronate liposome was used to deplete TAM. The blockade of VEGF-C/D with soluble VEGF receptor-3 markedly inhibited lymphangiogenesis and lymphatic metastasis in OUBC. In addition, the depletion of TAM with clodronate liposome exerted similar effects on OUBC.ConclusionVEGF-C/D are the main factors of lymphangiogenesis and lymphatic metastasis in bladder cancer. Moreover, TAM plays an important role in these processes by producing VEGF-C/D. The inhibition of lymphangiogenesis could provide another therapeutic target to inhibit lymphatic metastasis and recurrence in patients with invasive bladder cancer.
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45 ConclusionVEGF
46 MBT-2 cell line
47 ResultsThe
48 VEGF
49 VEGF receptor-3
50 VEGFR-3
51 addition
52 adenovirus
53 aim
54 angiogenesis
55 bladder cancer
56 bladder cancer model
57 bladder cancer patients
58 bladder tumors
59 blockade
60 blockade of VEGF
61 cancer
62 cancer model
63 cancer patients
64 cell lines
65 cells
66 clodronate liposomes
67 course
68 depletion
69 depletion of TAMs
70 disease progression
71 effect
72 effective therapeutic option
73 endothelial cells
74 factors
75 high levels
76 immunofluorescence
77 important role
78 infiltration
79 inhibition
80 inhibition of lymphangiogenesis
81 injection
82 intravesical injection
83 invasive bladder cancer
84 levels
85 lines
86 liposomes
87 lymph nodes
88 lymphangiogenesis
89 lymphatic metastasis
90 lymphatic vascular endothelial cells
91 lymphatic vessels
92 macrophages
93 main factors
94 manner
95 massive infiltration
96 mechanism
97 metastasis
98 microenvironment
99 model
100 nodes
101 options
102 paracrine manner
103 pathway
104 patients
105 primary tumor
106 process
107 progression
108 receptor 3
109 recurrence
110 relationship
111 role
112 similar effects
113 soluble VEGF receptor-3
114 study
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116 therapeutic options
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