The ICAM1 Knockout NCI-H1975 Polyclonal Cells are a CRISPR/Cas9-edited heterogeneous population derived from human lung adenocarcinoma NCI-H1975 cells, designed for loss-of-function studies of ICAM1. As polyclonal knockout cells, they retain genetic diversity from the editing pool, minimizing clonal bias while enabling robust population-level analyses. This model avoids the need for single-cell cloning, offering a practical tool for dissecting ICAM1-dependent mechanisms in oncology and immunology research.
NCI-H1975 is an epithelial non-small cell lung adenocarcinoma line with endogenous EGFR mutations L858R and T790M, which drive constitutive kinase activity and resistance to first-generation EGFR inhibitors. Its adherent growth and well-defined mutational landscape make it a standard model for studying EGFR signaling crosstalk with adhesion and inflammatory pathways. The epithelial nature of NCI-H1975 supports assays such as adhesion, migration, and invasion in a cancer-relevant microenvironment.
ICAM-1 is a transmembrane adhesion glycoprotein of the immunoglobulin superfamily that mediates leukocyte firm adhesion and transendothelial migration by binding ??2 integrins LFA-1 (CD11a/CD18) and Mac-1 (CD11b/CD18), as well as fibrinogen and hyaluronan. Its expression is induced by pro-inflammatory cytokines TNF-??, IL-1??, and IFN-?? via NF-??B and AP-1 transcription factors. Ligand engagement triggers intracellular signaling involving Src kinases, Rho GTPases, and ERM proteins, leading to actin cytoskeleton reorganization, endothelial junction disassembly, and production of pro-inflammatory mediators. ICAM-1 thus integrates inflammatory stimuli with leukocyte trafficking and tissue remodeling processes.
In the NCI-H1975 background, oncogenic EGFR signaling may converge with ICAM-1 pathways to influence tumor?Cimmune interactions, metastasis, and drug sensitivity. ICAM1 disruption in this EGFR-mutant adenocarcinoma enables dissection of adhesion-dependent signaling that could cooperate with EGFR to promote cancer cell survival and dissemination. This knockout model is particularly valuable for investigating how loss of epithelial ICAM-1 affects the tumor microenvironment and inflammatory cross-talk.
This polyclonal knockout product is applicable to a range of assays, including flow cytometric verification of ICAM-1 surface loss, western blotting, static cell adhesion assays, and transwell migration/invasion studies. It supports neutrophil?Cepithelial adhesion experiments, immunofluorescence, RT-qPCR for ICAM1 mRNA, and ELISA for soluble ICAM-1. Researchers can also utilize these cells to study rhinovirus entry, which requires ICAM-1, and to screen for anti-inflammatory or anti-metastatic compounds. For further information, please contact Ascent Research.
