In Stock Cell Lines
Homo sapiens (Human)
Oral cavity (tongue)
Adherent
The NFKBIA Knockout CAL-27 Cell Line is a CRISPR/Cas9-edited human oral squamous cell carcinoma model with disruption of the NFKBIA gene, which encodes the NF-??B inhibitor I??B??. Loss of I??B?? results in constitutive nuclear NF-??B activity, driving pro-survival and proliferative gene expression programs. This engineered line is ideal for analyzing the IKK/I??B??/NF-??B axis and its target genes such as CCND1 and BCL2. Applications include reporter assays, immunofluorescence for p65 translocation, and functional studies of migration, invasion, and drug resistance in oral cancer research.
PAPSS2 Knockout K562 Polyclonal Cells
Cat. No. ARG19229
HMGCL Knockout A2780 Polyclonal Cells
Cat. No. ARG29130
CD44 Knockout DLD-1 Polyclonal Cells
Cat. No. ARG43586
CBR3 Knockout HEK293T Polyclonal Cells
Cat. No. ARG42707
NT5C2 Knockout HEK293T Polyclonal Cells
Cat. No. ARG4471
LC-2/ad
Cat. No. ARC0438
The NFKBIA Knockout CAL-27 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the human tongue squamous cell carcinoma line CAL-27, with targeted disruption of the NFKBIA gene (Homo sapiens). This stable loss-of-function model enables investigation of I??B?? functions in signal transduction and cancer biology. The gene editing was performed via CRISPR/Cas9-mediated genome modification, and the cell population is supplied for immediate culture and assay deployment.
The parental CAL-27 cell line, established from a tongue squamous cell carcinoma of a 56-year-old male, is an adherent epithelial model widely used in oral cancer research. It retains key signaling receptors such as TNFR, IL1R, and TLRs, providing a clinically relevant context to study inflammatory and survival pathways in head and neck cancer.
NFKBIA encodes I??B??, the primary cytoplasmic inhibitor of NF-??B transcription factors. I??B?? sequesters NF-??B dimers, predominantly p50/RELA (p65), in an inactive state. Pathway activation by TNF, IL-1, or LPS stimulates the IKK complex (IKK??, IKK??, IKK??) to phosphorylate I??B??, leading to its ??-TrCP-mediated ubiquitination and degradation. Liberated NF-??B dimers translocate to the nucleus and induce target genes such as CCND1, BCL2, BCL2L1, IL6, TNF, MMP9, and VEGFA. NFKBIA transcription is itself NF-??B-dependent, establishing an auto-regulatory loop. In the knockout, I??B?? absence results in constitutive nuclear NF-??B localization and persistent transcriptional activity, driving pro-survival and pro-inflammatory gene expression.
In CAL-27 oral cancer cells, NFKBIA knockout amplifies tumorigenic traits by sustaining NF-??B-mediated proliferation (via CCND1), apoptosis resistance (via BCL2 family members), and invasive signaling (via MMP9, VEGFA). This model recapitulates the hyperactive NF-??B state found in aggressive oral squamous cell carcinomas, thus facilitating studies of oncogenic signaling and therapeutic vulnerabilities.
Applications include mechanistic dissection of NF-??B pathway dynamics, drug screening for anti-inflammatory or anti-cancer agents, and functional analyses of tumor microenvironment interactions. Compatible assays encompass Western blotting for NFKBIA, phospho-p65, and IKK; RT-qPCR for target genes; NF-??B reporter assays; immunofluorescence for p65 translocation; flow cytometry for apoptosis/cell cycle; colony formation; transwell migration/invasion; and drug sensitivity profiling. For technical inquiries, contact Ascent Research.
