The CD55 Knockout NCI-H1975 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to ablate CD55 expression in the NCI-H1975 human lung adenocarcinoma cell line. By introducing targeted gene disruptions via CRISPR/Cas9, this polyclonal pool eliminates functional CD55 protein, providing a versatile loss-of-function model. The polyclonal format preserves genetic heterogeneity while depleting the target gene product, making it suitable for population-level studies of CD55-dependent processes.
The NCI-H1975 cell line is a human lung adenocarcinoma model derived from a non-small cell lung cancer patient. It harbors an activating EGFR L858R mutation, which drives oncogenic signaling and sensitivity to EGFR inhibitors. This epithelial cell line is extensively employed in cancer biology and drug resistance studies, providing a disease-relevant context for CD55 knockout experiments.
CD55 is a GPI-anchored complement regulatory protein that accelerates the decay of C3 and C5 convertases (C4b2a and C3bBb), blocking membrane attack complex (C5b-9) formation and preventing cell lysis. It binds C3b and C4b, and interacts with CD97 and viral receptors for echovirus and coxsackievirus. This regulatory action dampens complement activation, reducing opsonization and anaphylatoxin generation. CD55 transcription is induced by TNF-??, IL-1??, and IFN-?? via NF-??B and Sp1, linking inflammation to complement resistance.
In NCI-H1975 cells, CD55 overexpression contributes to immune evasion by protecting against complement-dependent cytotoxicity. Knockout of CD55 sensitizes these cells to complement-mediated lysis, enabling detailed study of complement regulators in cancer immune surveillance. The model also facilitates investigation of CD55 as a viral entry receptor and screening of virus-receptor interaction inhibitors. The combination of an oncogenic driver mutation and loss of a complement checkpoint creates a platform to explore crosstalk between EGFR signaling and innate immunity.
Key applications include complement-dependent cytotoxicity assays (using normal human serum), flow cytometry and immunofluorescence to assess CD55 loss and C3b/MAC deposition, and co-immunoprecipitation with CD97 or C3b binding studies. The polyclonal knockout cells are suitable for evaluating therapeutic antibody-mediated CDC in cancer immunotherapy and for echovirus/coxsackievirus infection assays. Complementary techniques such as western blotting and RT-qPCR can confirm knockout and interrogate pathway changes. Contact Ascent Research for further details.
