The ITFG2 Knockout NCI-H1975 Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the ITFG2 gene in the NCI-H1975 human lung adenocarcinoma cell line. This polyclonal pool provides a genetically diverse loss-of-function model, circumventing clonal artifacts and enabling robust functional analysis of ITFG2. The gene disruption is achieved through CRISPR/Cas9-mediated genome editing, creating a versatile tool for studying ITFG2’s role in integrin signaling and cancer biology.
NCI-H1975 is a human non-small cell lung adenocarcinoma cell line that serves as a well-established preclinical model. It exhibits an adherent epithelial phenotype and retains key oncogenic characteristics, including mutations in the EGFR pathway, making it highly relevant for investigating molecular mechanisms of lung tumorigenesis. The cell line’s stable growth and extensive characterization facilitate its use in knockout studies to elucidate pathways governing cancer cell adhesion, migration, and survival.
ITFG2 encodes an integrin-associated protein characterized by FG-GAP repeats, which localizes to cell-extracellular matrix adhesion sites. Its activity is triggered by ECM ligands and pro-inflammatory cytokines such as TNF-alpha, which engage integrin receptors. ITFG2 directly interacts with integrin ?? subunits like ITGAL (CD11a) and ?? subunits, forming complexes with the adaptor protein talin. These interactions promote the phosphorylation and activation of focal adhesion kinase (FAK) and SRC tyrosine kinases. Downstream, FAK and SRC drive actin cytoskeleton remodeling and stimulate the PI3K-Akt signaling cascade, ultimately regulating cell migration, adhesion, and survival. Additionally, ITFG2 may contribute to immune cell function through integrin-mediated processes.
In NCI-H1975 lung adenocarcinoma cells, ITFG2 is anticipated to support integrin-dependent adhesion and migration, which are critical for tumor invasion and metastasis. Disruption of ITFG2 expression in this model allows researchers to dissect its specific contributions to malignant phenotypes, including anchorage-independent growth and motility. The knockout cells provide a platform to evaluate how loss of ITFG2 alters integrin-FAK-SRC-PI3K-Akt signaling and to identify synthetic lethalities with targeted therapies against these pathways.
This product is applicable to a wide range of functional genomics and cancer biology studies. It enables characterization of ITFG2 in lung adenocarcinoma progression, validation of drug candidates targeting integrin and downstream kinase pathways, and screening for modulators of adhesion-dependent signaling. Representative experimental approaches include Western blotting and RT-qPCR for expression analysis, immunofluorescence to visualize focal adhesion complexes, cell adhesion and migration assays, flow cytometry for integrin surface levels, and phospho-FAK ELISA to quantify FAK activation. For further technical details and ordering information, please contact Ascent Research.
