Please use this identifier to cite or link to this item: https://scidar.kg.ac.rs/handle/123456789/9135
Title: Deletion of IL-33R attenuates VEGF expression and enhances necrosis in mammary carcinoma
Authors: Milosavljevic, Milos
Jovanovic I.
Pejnović, Nada
Mitrovic M.
Arsenijevic, Nebojsa
Markovic B.
Lukic, Miodrag
Issue Date: 2016
Abstract: Interleukin-33 (IL-33)/IL-33 receptor (IL-33R, ST2) signaling pathway promotes mammary cancer growth and metastasis by inhibiting anti-tumor immunity. However, the role of IL-33/IL-33R axis in neoangiogenesis and tumor necrosis is not elucidated. Therefore, the aim of this study was to investigate the role of IL-33/IL-33R axis in mammary tumor necrosis. Deletion of IL-33R (ST2) gene in BALB/c mice enhanced tumor necrosis and attenuated tumor growth in 4T1 breast cancer model, which was associated with markedly decreased expression of vascular endothelial growth factor (VEGF) and IL-33 in mammary tumor cells. We next analyzed IL-33, IL-33R and VEGF expression and microvascular density (MVD) in breast tumors from 40 female patients with absent or present tumor necrosis. We found significantly higher expression of IL-33, IL-33R and VEGF in breast cancer tissues with absent tumor necrosis. Both, IL-33 and IL-33R expression correlated with VEGF expression in tumor cells. Further, VEGF expression positively correlated with MVD in perinecrotic zone. Taking together, our data indicate that IL-33/IL-33R pathway is critically involved in mammary tumor growth by facilitating expression of pro-angiogenic VEGF in tumor cells and attenuating tumor necrosis. These data add an unidentified mechanism by which IL-33/IL-33R axis facilitates tumor growth.
URI: https://scidar.kg.ac.rs/handle/123456789/9135
Type: article
DOI: 10.18632/oncotarget.7635
SCOPUS: 2-s2.0-84975511059
Appears in Collections:Faculty of Medical Sciences, Kragujevac

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