TI - IL-1beta induces activation of NFkappaB in HC-11/R1 mammary epithelial cells . AB - Based on the results from the in vivo studies , we hypothesised that IL-1beta acts on the mammary epithelial cells to contribute to the formation of iFGFR1 -induced hyperplastic lesions . Therefore , initial studies were performed to ascertain the ability of mammary epithelial cells to respond to IL-1beta stimulation by examining activation of downstream signalling pathways using the HC-11/R1 cell line described previously . Initial studies using both quantitative RT-PCR and immunoblot analysis demonstrated that the HC-11/R1 cells express the IL-1 receptor ( IL-1R ) ( data not shown ) . Further studies were performed using both dose-response and time-course analyses to examine the activation of nuclear factor ( NF ) kappaB , which is a key downstream target of IL-1beta in other cell types [26] . Treatment of HC-11/R1 cells with recombinant murine ( rm ) IL-1beta resulted in a rapid induction of PHOSphorylation of the p65 subunit of NFkappaB within 15 minutes of treatment as shown by immunoblot analysis ( Figures 3a , b ) . Based on the observation that 5 ng/ml of rmIL-1beta was within the linear range of response ( Figure 3a ) , this concentration was used for the remainder of the studies . These results demonstrate that the HC-11/R1 mammary epithelial cell line responds to rmIL-1beta treatment by activating a downstream signalling pathway .