The IL1R1 Knockout MCF-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the MCF-7 human breast adenocarcinoma cell line, featuring targeted disruption of the IL1R1 gene. This loss-of-function model allows researchers to interrogate IL-1 receptor type 1 signaling in the absence of clonal selection, providing a population-level representation of gene knockout effects.
The parental MCF-7 line is an estrogen receptor-positive (ER+), progesterone receptor-positive (PR+) breast adenocarcinoma model with epithelial morphology and wild-type p53. Widely used in hormone-responsive cancer research, MCF-7 cells exhibit well-characterized signaling networks, making them a suitable platform for investigating gene function in ER+ breast cancer biology and therapy response.
IL1R1 encodes the primary receptor for IL-1?? and IL-1??. Ligand engagement triggers recruitment of IL1RAP and association with the adaptor MyD88, which subsequently activates IRAK1 and IRAK4. These kinases interact with TRAF6, leading to TAK1 (in complex with TAB1 and TAB2) activation. TAK1 phosphorylates the IKK complex to induce NF-??B nuclear translocation, while simultaneously activating MAPK cascades (p38, JNK). This signaling drives expression of downstream targets including pro-inflammatory cytokines IL6, IL8, and TNF; chemokines CXCL1 and CXCL8; COX-2; and matrix metalloproteinases. Negative regulation is exerted by the endogenous antagonist IL-1Ra.
In MCF-7 cells, IL1R1 knockout enables direct analysis of IL-1 signaling contributions to tumor cell-autonomous inflammation, proliferation, and survival. This model is particularly valuable for studying crosstalk between inflammatory pathways and hormone-responsive signaling in ER+ breast cancer, and for understanding how IL-1/NF-??B/MAPK networks influence tumor microenvironment interactions and therapeutic resistance.
Key applications include Western blot detection of phosphorylated NF-??B components (p-p65, p-I??B??), RT-qPCR for IL-6 and IL-8, MAPK phospho-profiling, NF-??B luciferase reporter assays, and co-immunoprecipitation of IL1R1/IL1RAP complexes. Functional assays such as drug sensitivity testing with anakinra (IL-1 receptor antagonist) and IL-1-stimulated proliferation assays further validate pathway dependency. The polyclonal pool is also suitable for compound screening targeting the IL-1/NF-??B axis. For additional information or custom requests, please contact Ascent Research.
