The EDIL3 Knockout NCI-H1975 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the NCI-H1975 human lung adenocarcinoma cell line, designed for loss-of-function studies of the EDIL3 gene. This polyclonal knockout pool provides a heterogeneous cell population with EDIL3 ablation, enabling robust phenotypic analysis without clonal selection biases. The gene disruption is generated via CRISPR/Cas9, and the product is supplied as a polyclonal population suitable for functional assays.
The NCI-H1975 cell line is a lung adenocarcinoma model originating from a female non-small cell lung cancer patient. These cells carry EGFR L858R and T790M mutations, which confer sensitivity and resistance to EGFR tyrosine kinase inhibitors, respectively. NCI-H1975 cells are widely used to study oncogenic signaling and drug resistance in EGFR-mutant lung cancer.
EDIL3 encodes a secreted extracellular matrix protein that promotes cell adhesion, migration, and survival through integrin binding. It interacts with integrin ??V??3 and ??V??5, and extracellular matrix components collagen and fibronectin. Upon engagement, EDIL3 activates FAK and SRC kinases, which phosphorylate AKT and ERK, enhancing survival and motility. EDIL3 also modulates NF-??B signaling to regulate inflammation and angiogenesis. Its expression is induced by VEGF, TGF-??, TNF-??, and IL-1??. Thus, EDIL3 orchestrates a signaling network involving FAK, SRC, AKT, ERK, and NF-??B to coordinate adhesion, migration, survival, and inflammatory responses.
In NCI-H1975 cells with constitutive EGFR activation, EDIL3 knockout enables dissection of crosstalk between integrin and EGFR pathways. Loss of EDIL3 allows assessment of its role in adhesion, migration, and survival specifically in the context of EGFR L858R/T790M-driven tumor biology. This model is particularly relevant for investigating how EDIL3 influences drug sensitivity and metastatic potential, as EDIL3 has been implicated in resistance to targeted therapies. The polyclonal nature ensures representative phenotypic assessment without clonal variation artifacts.
These knockout cells are suited for cell adhesion, migration, and invasion assays, as well as Western blot detection of phospho-FAK, phospho-AKT, and phospho-ERK. Immunofluorescence and flow cytometry can be used to evaluate integrin expression changes. RNA-seq enables transcriptome-wide analysis of EDIL3 loss in EGFR-mutant NSCLC. Additionally, the cells provide a platform to study EDIL3-mediated drug responses and tumor microenvironment interactions. For more information, contact Ascent Research.
