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CXCL7 介导的人乳腺癌细胞中淋巴管生成因子 VEGF-C、VEGF-D 的刺激作用。

CXCL7-Mediated Stimulation of Lymphangiogenic Factors VEGF-C, VEGF-D in Human Breast Cancer Cells.

机构信息

Department of Surgery, Wayne State University, Detroit, MI 48201, USA.

出版信息

J Oncol. 2010;2010:939407. doi: 10.1155/2010/939407. Epub 2010 Jun 22.

DOI:10.1155/2010/939407
PMID:20652010
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2906176/
Abstract

Increased expression of lymphangiogenesis factors VEGF-C/D and heparanase has been correlated with the invasion of cancer. Furthermore, chemokines may modify matrix to facilitate metastasis, and they are associated with VEGF-C and heparanase. The chemokine CXCL7 binds heparin and the G-protein-linked receptor CXCR2. We investigated the effect of CXCR2 blockade on the expression of VEGF-C/D, heparanase, and on invasion. CXCL7 siRNA and a specific antagonist of CXCR2 (SB225002) were used to treat CXCL7 stably transfected MCF10AT cells. Matrigel invasion assays were performed. VEGF-C/D expression and secretion were determined by real-time PCR and ELISA assay, and heparanase activity was quantified by ELISA. SB225002 blocked VEGF-C/D expression and secretion (P < .01). CXCL7 siRNA knockdown decreased heparanase (P < .01). Both SB225002 and CXCL7 siRNA reduced the Matrigel invasion (P < .01). The MAP kinase signaling pathway was not involved. The CXCL7/CXCR2 axis is important for cell invasion and the expression of VEGF-C/D and heparanase, all linked to invasion.

摘要

淋巴管生成因子 VEGF-C/D 和乙酰肝素酶的表达增加与癌症的侵袭有关。此外，趋化因子可能修饰基质以促进转移，并且它们与 VEGF-C 和乙酰肝素酶有关。趋化因子 CXCL7 与肝素和 G 蛋白偶联受体 CXCR2 结合。我们研究了 CXCR2 阻断对 VEGF-C/D、乙酰肝素酶表达和侵袭的影响。使用 CXCL7 siRNA 和 CXCR2 的特异性拮抗剂 (SB225002) 处理 CXCL7 稳定转染的 MCF10AT 细胞。进行 Matrigel 侵袭测定。通过实时 PCR 和 ELISA 测定法确定 VEGF-C/D 的表达和分泌，并通过 ELISA 定量测定乙酰肝素酶活性。SB225002 阻断 VEGF-C/D 的表达和分泌 (P <.01)。CXCL7 siRNA 敲低降低了乙酰肝素酶 (P <.01)。SB225002 和 CXCL7 siRNA 均减少了 Matrigel 侵袭 (P <.01)。MAP 激酶信号通路不参与其中。CXCL7/CXCR2 轴对于细胞侵袭以及与侵袭相关的 VEGF-C/D 和乙酰肝素酶的表达很重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d8/2906176/5728441bc255/JO2010-939407.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d8/2906176/e3079d6ed198/JO2010-939407.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d8/2906176/37d482ea4cb3/JO2010-939407.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d8/2906176/edd41ef9bdfc/JO2010-939407.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d8/2906176/aed525157998/JO2010-939407.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d8/2906176/5728441bc255/JO2010-939407.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d8/2906176/e3079d6ed198/JO2010-939407.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d8/2906176/37d482ea4cb3/JO2010-939407.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d8/2906176/edd41ef9bdfc/JO2010-939407.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d8/2906176/aed525157998/JO2010-939407.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d8/2906176/5728441bc255/JO2010-939407.005.jpg

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