Macrophage conditioned medium (MϕCM) containing elevated levels of cytokines TNF-α, IL-1β and IL-6 had a differential effect on non-invasive (MCF7) and highly invasive (MDA-MB-231) breast cancer cell lines.
Methods Women (N = 315; 209 with breast cancer and 106 in the control group) were recruited at the time of their work-up for breast cancer; they completed the baseline questionnaire, interview, and blood draw (lipopolysaccharide-stimulated production of interleukin [IL] -6, tumor necrosis factor-α, and IL-1β).
Our data reveal the association between genetic polymorphisms of IL-1 and BC susceptibility in the Chinese Han population and indicates that IL-1 polymorphisms are closely associated with tumor markers and IL-1β protein expression in BC patients.
Our results show that breast cancer cells migrate to human bone tissue-conditioned medium in association with increasing levels of leptin and IL-1β, and colonize the bone marrow adipose tissue compartment of cultured fragments.
Our results suggest that: (a) the IL-1beta gene is a primary target of RA receptors in HMEC; (b) the enhanced expression of the IL-1beta gene does not mediate the RA-induced growth arrest of HMEC; and (c) the expression of the IL-1beta gene is low or absent in all three human breast carcinoma cell lines examined, but the defect in the IL-1beta signaling pathway may be different in ER positive versus ER negative carcinoma cells.
Response to commentary article: "The association between Interleukin-1β gene rs1143634 polymorphism and the risk of breast cancer by Bei Wang, Fenlai Yuan".
Results demonstrate that macrophage production of IL-1β plays an important role in the migration of breast cancer cells and their adhesion to, and transmigration across, blood and lymphatic endothelial cells.
Serum cytokine levels of interleukin-1beta, -6, -8, tumour necrosis factor-alpha and vascular endothelial growth factor in breast cancer patients treated with tamoxifen and supplemented with co-enzyme Q(10), riboflavin and niacin.
Taken together, we have demonstrated a functional IL-1 system in breast cancer and observed an inverse correlation between IL-1alpha and sex steroid receptor expression.
The cytokine interleukin-1 (IL-1) can inhibit growth of breast cancer cells in culture and promote cellular differentiation in synergism with other growth factors.
The frequency of the <i>T</i> allele of <i>IL-1β-C31T</i> polymorphism in breast cancer cases was significantly higher than that in the controls (56.1% vs. 47.9%).
Therefore, the combination of the expression of IL-1β, IL-6 and IL-10 may serve as promising biomarkers of MICs with prognostic significance, contributing to a better characterization of breast carcinomas microenvironment.
These findings establish that targeting IL1β-NFKB/CREB-Wnt signalling should be considered for adjuvant therapy to prevent breast cancer bone metastasis.
These studies define the role for IL-1β in the metastatic progression of breast cancer and highlight the need to control PI, a pervasive inflammatory condition in older patients.
Tumor/stromal IL1B and IL1 receptor 1 (IL1R1) expression was assessed in patient samples and effects of the IL1R antagonist, Anakinra, or the IL1B antibody canakinumab on tumor growth and spontaneous metastasis were measured in a humanized mouse model of breast cancer bone metastasis.
Using RNA interference, we have reduced the expression of COX-2 in the highly malignant breast cancer cell line MDA-MB-231 below detectable levels in response to interleukin-1 beta or 12-O-tetradecanoylphorbol-13-acetate treatment.