The ITGA1 Knockout NCI-H1975 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the NCI-H1975 human lung adenocarcinoma line. This product offers a heterogeneous loss-of-function model in which the ITGA1 gene is disrupted across the cell pool, suitable for pooled functional studies and population-averaged phenotypic analyses. The polyclonal format avoids clonal artifacts and reflects a range of editing outcomes consistent with standard CRISPR/Cas9 delivery.
NCI-H1975 is a well-characterized non-small cell lung cancer (NSCLC) model of lung adenocarcinoma origin, extensively used for investigating tumor cell signaling, drug sensitivity, and metastasis. Its adherent epithelial nature and retained dependency on EGFR-driven pathways make it a relevant host for examining integrin-mediated processes in NSCLC biology.
ITGA1 encodes the integrin ??1 subunit, which pairs with ??1 integrin (ITGB1) to form the ??1??1 collagen/laminin receptor. Ligand binding activates focal adhesion kinase (FAK) and SRC, triggering PI3K/AKT1 and MAPK1/3 (ERK1/2) cascades along with RhoA-dependent cytoskeletal changes. Upstream regulation involves TGFB1-induced transcription and direct activation by ECM components including collagen types I/IV, laminin-111, and fibronectin. The receptor also couples to the adaptor Shc. Knockout of ITGA1 abolishes ??1??1-mediated adhesion, resulting in attenuated FAK phosphorylation, reduced AKT and ERK1/2 activity, and impaired cell migration and survival on collagen/laminin matrices.
In NCI-H1975 cells, ITGA1 disruption is particularly valuable for dissecting integrin-dependent adhesion signaling in lung adenocarcinoma. NSCLC progression often involves dysregulated ECM interaction; thus, this model enables direct study of how ??1??1 integrin contributes to tumor cell invasion, matrix adhesion, and resistance to detachment-induced death. Additionally, the model can be combined with EGFR inhibitors to explore crosstalk between integrin and growth factor pathways relevant to treatment response.
Key applications include Western blot analysis of phospho-FAK and phospho-AKT, adhesion assays on collagen I or laminin-111, wound-healing migration, and Transwell invasion assays. Further uses encompass cell viability measurements under ECM stress, RNA sequencing of pathway alterations, and co-culture studies of tumor?Cstroma interactions. These tools support research into fibrosis-related cancer signaling, metastasis, and the tumor microenvironment. For further information, please contact Ascent Research.
