The CD55 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting CD55 in the HT29 colorectal adenocarcinoma line. This loss-of-function model abolishes decay-accelerating factor activity, enabling study of complement regulation and immune evasion. The polyclonal format retains genetic diversity, providing a robust representation of knockout phenotypes. Rigorous quality assurance confirms gene disruption.
HT29 is an epithelial colorectal adenocarcinoma line with TP53, APC, SMAD4, and BRAF V600E mutations, and is microsatellite stable. It undergoes enterocytic differentiation and mucin production under confluency or butyrate treatment, making it a relevant intestinal epithelial model for cancer biology and host-immune interactions.
CD55, a GPI-anchored decay-accelerating factor, inhibits C3 and C5 convertases by accelerating their decay, thereby preventing membrane attack complex assembly and complement-mediated lysis. Its expression is induced by TNF-alpha, IL-1, IL-6, and interferon-gamma via NF-kB and STAT3 signaling, and it interacts with C3b, C4b, factor B, factor D, CD97, and bacterial adhesins. CD55 knockout leads to uncontrolled complement activation, C3b deposition, MAC formation, and cell lysis, while also perturbing MAPK signaling and cytokine secretion (e.g., IL-8, IL-6). Thus, CD55 bridges complement regulation with immune signaling and epithelial homeostasis.
In the HT29 background, CD55 knockout disrupts a key tumor immune evasion strategy, enhancing susceptibility to complement-dependent cytotoxicity. The BRAF V600E mutation, combined with loss of DAF, offers a model to study how oncogenic signaling intersects with complement resistance. This polyclonal system mimics intratumoral heterogeneity, enabling investigation of CD55??s role in cytokine responses, bacterial adhesion, and the interplay between complement regulation and colorectal cancer progression.
Applications include complement-dependent cytotoxicity assays (LDH release, MTT), flow cytometry for C3b deposition, immunofluorescence for MAC, and drug screening for complement inhibitors. Further uses encompass host-pathogen interaction studies, cytokine ELISA, RT-qPCR for complement regulatory genes, and paroxysmal nocturnal hemoglobinuria modeling. This knockout product is an essential tool for validating immunotherapy targets and exploring complement biology in cancer. For additional information, contact Ascent Research.
