CD55 Knockout NCI-H1299 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the human non-small cell lung carcinoma (NSCLC) cell line NCI-H1299. This product comprises a heterogeneous pool of cells with targeted disruption of the CD55 gene, providing a physiological loss-of-function model for investigating complement regulatory mechanisms and tumor immune evasion. Unlike monoclonal knockout lines, the polyclonal format preserves the genetic diversity of the edited population, which can be advantageous for studies requiring representation of multiple clonal editing events.
The parental NCI-H1299 cell line is a widely utilized model of lung adenocarcinoma, originally established from a lymph node metastasis. It carries an activating KRAS mutation and lacks functional p53 protein due to a homozygous deletion, recapitulating two of the most common genetic alterations in NSCLC. These characteristics make NCI-H1299 particularly valuable for research on oncogenic signaling, metastasis, and therapeutic resistance. The cells exhibit adherent growth and are suitable for a range of in vitro assays, including drug sensitivity testing and co-culture experiments.
CD55, also known as decay-accelerating factor, is a glycosylphosphatidylinositol-anchored membrane protein that functions as a key inhibitor of the complement cascade. It accelerates the decay of both C3 and C5 convertases, thereby limiting the deposition of C3b and the formation of the membrane attack complex (C5b-9) on host cells. CD55 expression is regulated by multiple pro-inflammatory stimuli, including TNF-?? and IL-1??, via transcription factors such as NF-??B and AP-1. In addition to its complement-regulatory role, CD55 interacts with the adhesion G protein-coupled receptor CD97 (ADGRE5), modulating downstream signaling through Src family kinases, PI3K/AKT, and ERK1/2 pathways. This dual functionality links CD55 to both innate immune protection and cellular responses related to survival and adhesion.
In the NCI-H1299 background, CD55 knockout eliminates the cell’s primary defense against complement-mediated lysis, rendering these cells highly susceptible to complement attack. This sensitization is expected to increase C3b deposition and generation of C5b-9 upon exposure to complement factors. Furthermore, disruption of CD55-CD97 interactions may impair Src-PI3K-AKT-ERK signaling, potentially reducing anti-apoptotic signals and altering migratory capacity. These molecular changes provide a relevant platform to probe the intersection of complement regulation and oncogenic signaling in a KRAS-mutant, p53-null lung adenocarcinoma context.
Researchers can employ CD55 Knockout NCI-H1299 Polyclonal Cells in a variety of experimental workflows, including complement-mediated cytotoxicity assays to evaluate the efficacy of complement-activating therapies, flow cytometric analysis of C3b deposition and CD55 expression, and western blotting for downstream signaling components such as phosphorylated AKT and ERK. Cell viability and migration assays, as well as co-culture models with immune effectors, can further elucidate the role of CD55 in tumor immune evasion and metastatic potential. This knockout tool is also suitable for high-throughput screening of compounds that enhance complement-dependent cytotoxicity. For technical inquiries and additional product information, please contact Ascent Research.
