However, combination of IL-1B C-allele (CT or CC) and IL-1RN *2-allele containing genotypes significantly decreased the risk of breast cancer (OR = 0.6, 95% CI = 0.39-0.99).
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.
Genetic variation in pro-inflammatory cytokines (interleukin-1beta, interleukin-1alpha and interleukin-6) associated with the aggressive forms, survival, and relapse prediction of breast carcinoma.
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.
In this study, we compared the mechanism(s) by which IL-1 beta induces collagenase gene expression in two very different cells, normal human foreskin fibroblasts (HFFs) and an aggressive breast cancer cell line, BC-8701 cells.
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.