The IKBKB Knockout DLD-1 Polyclonal Cells represent a pooled population of human DLD-1 colorectal adenocarcinoma cells edited via CRISPR/Cas9 to disrupt the IKBKB gene, encoding the IKK?? kinase. This loss-of-function model enables study of canonical NF-??B signaling in a polyclonal background, minimizing clonal selection artifacts. The mixed knockout pool is supplied at early passage and is designed for in vitro investigation of IKK??-dependent cellular processes.
The parental DLD-1 line originated from a Dukes’ type C colorectal adenocarcinoma and serves as a well-established epithelial model for colorectal cancer. These cells exhibit dysregulated proliferation, survival, and invasion pathways, making them particularly suitable for examining oncogenic signaling and therapeutic responses. DLD-1’s robust growth characteristics and compatibility with standard molecular biology techniques facilitate gene-editing and downstream analyses.
IKBKB encodes the catalytic subunit of the IKK complex, essential for canonical NF-??B signaling. Stimuli through TNFR1, IL-1R, or TLRs converge on adaptors TRAF6 and RIPK1 and the kinase TAK1 to activate the IKK complex??comprising IKK??, IKK?? (CHUK), and NEMO (IKBKG). Activated IKK?? phosphorylates I??B?? (NFKBIA), triggering its degradation and releasing NF-??B dimers (p65/RELA and p50/NFKB1) to enter the nucleus and drive transcription of targets such as IL6, TNF, IL8, and BCL2. Molecular chaperones HSP90 and CDC37 also interact with IKK??, influencing its stability and function.
In colorectal cancer, NF-??B signaling promotes tumorigenesis, inflammation, and chemoresistance. IKBKB knockout in DLD-1 cells disrupts this pathway, enabling dissection of IKK??-specific roles in proliferation, apoptosis evasion, and migration. The model separates canonical NF-??B from IKK??-dependent non-canonical signaling and allows pharmacological testing of IKK?? inhibitors. It also aids in studying interactions with other colorectal cancer mutations and drug resistance.
Applications include Western blotting for IKK?? and phospho-I??B??, RT?qPCR for downstream targets (IL6, TNF), NF???B luciferase reporter assays, and p65 immunofluorescence. Functional studies such as MTT viability, caspase?3/7 apoptosis, and migration assays are supported, along with drug sensitivity screening using IKK??-targeted compounds. The cells are suitable for high?content analysis and mechanistic investigation of NF???B in colorectal cancer. For further technical information, please contact Ascent Research.
