The CD14 Knockout CAL-27 Polyclonal Cells consist of a CRISPR/Cas9-edited heterogeneous cell pool derived from the CAL-27 human oral squamous cell carcinoma line, featuring a targeted disruption of the CD14 gene. This loss-of-function model supports dissection of CD14-mediated innate immune pathways without single-cell cloning artifacts. The polyclonal format captures multiple edit outcomes, reflecting population-level gene ablation.
CAL-27 is an adherent epithelial line from a tongue squamous cell carcinoma, widely employed in oral cancer research. Its malignant phenotype and epithelial origin make it suitable for studying tumor cell responses to inflammatory signals, migration, and apoptosis. The cell line provides a relevant platform for examining how bacterial sensing pathways intersect with oncogenic processes.
CD14 operates as a glycosylphosphatidylinositol-anchored co-receptor for bacterial lipopolysaccharide (LPS), presenting LPS to the TLR4/MD-2 complex. Ligand engagement triggers MyD88- and TRIF-dependent signaling, leading to IKK complex activation, NF-??B nuclear translocation, and MAPK pathway stimulation. Transcription factors NF-??B and AP-1 then induce proinflammatory cytokines including IL-6, IL-8, and TNF-??. Upstream regulators such as LPS, TNF-??, and IL-1?? enhance CD14 expression via PU.1. LBP facilitates LPS transfer to CD14, and downstream adaptors MyD88, IRAK4, and TRAF6 relay signals, while SHIP and PI3K modulate signaling intensity.
In the CAL-27 oral cancer context, CD14 may link microbial stimulation to disease progression. LPS from oral microbiota can drive cytokine release, fostering a tumor-permissive microenvironment. Knocking out CD14 in this squamous carcinoma line enables dissection of how innate immune receptors influence malignant behaviors such as proliferation, motility, and apoptosis resistance. This model is pivotal for evaluating infection-inflammation-cancer axes in oral oncology.
This polyclonal knockout product is suited for functional assays including ELISA-based measurement of IL-6 and IL-8 secretion, NF-??B luciferase reporter assays, and Western blot analysis of phosphorylated p65, TLR4, and MyD88. Flow cytometry confirms CD14 loss, while LPS-induced apoptosis and scratch wound healing assays quantify cellular responses. Applications extend to studying sepsis, bacterial infection, inflammatory diseases, and drug resistance mechanisms in cancer. For further technical inquiries, please contact Ascent Research.
