The IL1B Knockout DLD-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human colorectal adenocarcinoma cell line DLD-1, engineered for loss-of-function studies of the interleukin-1 beta (IL1B) gene. This polyclonal pool enables robust investigation of IL1B-dependent signaling and its contributions to inflammation-associated colorectal cancer biology.
DLD-1 cells are a well-characterized epithelial model of colorectal adenocarcinoma, bearing mutations in APC, TP53, and KRAS, which recapitulate key oncogenic drivers of colorectal tumorigenesis. These cells retain epithelial morphology and are widely employed for studying tumor cell proliferation, migration, and drug responses in the context of a genetically unstable background.
IL1B encodes the potent pro-inflammatory cytokine IL-1??, which, upon secretion, binds to the IL-1 receptor complex comprising IL1R1 and IL1RAP, leading to the recruitment of MyD88, IRAK1, IRAK4, and TRAF6. This initiates downstream activation of the IKK complex and NF-??B, as well as the JNK and p38 MAPK pathways, ultimately driving the transcription of inflammatory mediators such as IL6, IL8, COX2, and matrix metalloproteinases. Additionally, IL-1?? is regulated by the NLRP3 inflammasome and caspase-1-mediated processing, and can be induced by upstream signals including LPS, TNF-??, and autocrine IL-1??. Disruption of IL1B therefore blocks this central cytokine axis, impairing both autocrine and paracrine inflammatory amplification.
In the DLD-1 context, IL1B knockout provides a defined system to dissect the role of IL-1?? in colorectal cancer progression, where chronic inflammation drives tumor promotion, immune evasion, and metastasis. By abrogating IL-1?? secretion, this model allows researchers to delineate tumor-intrinsic effects from microenvironmental contributions, enabling studies on how IL-1 signaling shapes the inflammatory secretome that supports cancer cell survival and invasion.
These polyclonal knockout cells are suitable for a range of functional assays, including ELISA quantification of IL-1?? to confirm loss, western blotting, RT-qPCR, NF-??B reporter assays, cell proliferation, migration/invasion assays, and cytokine arrays. They serve as a valuable tool for investigating the IL-1??-driven inflammatory network in colorectal cancer, screening anti-inflammatory compounds targeting IL-1 signaling, and studying inflammasome activation in a disease-relevant background. For additional details, custom projects, or bulk orders, please contact Ascent Research.
