The CCDC71L Knockout NCI-H1975 Polyclonal Cells consist of a human NCI-H1975 lung adenocarcinoma epithelial cell population engineered with CRISPR/Cas9 to disrupt the CCDC71L gene. Supplied as polyclonal knockout cells, this model maintains heterogeneous gene-editing events across the population, enabling functional studies without clonal selection.
NCI-H1975 is a non-small cell lung cancer line established from a never-smoker female, harboring EGFR L858R and T790M kinase domain mutations and MET gene amplification. These oncogenic drivers render the cells highly dependent on EGFR and MET signaling, providing a clinically relevant model for studying targeted therapy resistance and NSCLC progression.
CCDC71L encodes a coiled-coil domain-containing protein predicted to mediate protein?Cprotein interactions, though its precise cellular role is uncharacterized. In the context of NCI-H1975, CCDC71L could potentially intersect with EGFR, KRAS, and MET signaling networks that govern cell proliferation and survival. Knockout likely abolishes its putative scaffolding functions, perturbing unidentified downstream pathways.
This knockout model enables dissection of CCDC71L??s contribution to NSCLC biology in a background of EGFR and MET activation. It facilitates investigation of CCDC71L-dependent effects on cellular growth, drug sensitivity, and signal transduction, and may uncover synthetic lethal interactions or compensatory mechanisms relevant to EGFR TKI-resistant NSCLC.
Typical applications include western blotting, RT-qPCR, proliferation and colony formation assays, migration/invasion studies, drug sensitivity profiling, co-immunoprecipitation, and RNA-seq. These cells support functional characterization of CCDC71L, identification of interaction partners, and evaluation as a therapeutic target. For further information, please contact Ascent Research.
