Skip to main content
Figure 5 | Breast Cancer Research

Figure 5

From: Contribution of CXCL12 secretion to invasion of breast cancer cells

Figure 5

Epidermal growth factor-induced in vivo invasion is dependent on CXCR4/CXCL12 paracrine signaling in the tumor microenvironment. (A) In vivo invasion assay performed by infusing 25 nM epidermal growth factor (EGF) and EGF + 0.5 μM CXCR4 inhibitor AMD3100 through microneedles inserted into the primary tumor to collect the invasive cell population over 4 hours. Neu-NDL = Neu deletion mutant (activated receptor). Data are means and SEM. ***P < 0.0005 by t-test, n = three to five mice per strain and five to seven needles per condition. (B) In vivo invasion assay performed with 25 nM EGF + control rat immunoglobulin G (IgG) antibody or EGF + colony-stimulating factor 1 receptor (CSF-1R) blocking antibody (αCSF-1R IgG) in the needles. Data are means and SEM. ***P < 0.0005 by t-test, n = three to five mice per strain and five to seven needles per condition. (C) In vitro wound healing assays in the absence (Buffer) or presence of 5 nM EGF (EGF). Data are means and SEM. *P < 0.05, **P < 0.005 and ***P < 0.0005 by t-test, n = 3 tumors per strain and at least 10 fields per condition. (D) In vitro wound healing assays were performed with confluent primary tumor tissue in the presence of buffer (Buffer), 5 nM EGF alone (EGF), 5 nM EGF with 100 nM AMD3100 (EGF + AMD3100), 5 nM EGF with 1 nM CXCL12 (EGF + CXCL12) or 1 nM CXCL12 alone (CXCL12). Data are means and SEM. **P < 0.005 by t-test, n = 3 tumors and at least 10 fields per condition.

Back to article page