The ITGB1 Knouckout DLD-1 Polyclonal Cells consist of a heterogeneous pool of DLD-1 colorectal adenocarcinoma cells engineered via CRISPR/Cas9-mediated disruption of the ITGB1 gene. As a polyclonal knockout population, this product contains a diverse array of genetic edits leading to functional loss of integrin beta-1, circumventing clonal selection biases. The preparation is optimized for pooled assays, enabling robust interrogation of collective cellular responses to ITGB1 deficiency in a cancer-relevant background.
The DLD-1 host cell line originates from human colorectal adenocarcinoma and harbors tumorigenic mutations in APC and TP53, faithfully recapitulating key genetic drivers of colorectal carcinogenesis. These epithelial cells maintain adherent junctional properties and a transformed phenotype, rendering them a well-characterized platform for studying cell?Cmatrix interactions. The mutant background provides oncogenic context for dissecting how integrin signaling intersects with Wnt pathway dysregulation and compromised DNA damage responses.
ITGB1 encodes the beta-1 integrin subunit, which heterodimerizes with alpha integrins (ITGA1?C6, ITGAV) to form receptors for fibronectin, collagen, and laminin. Ligand engagement activates the adaptors talin and kindlin, inducing focal adhesion kinase (FAK) and SRC phosphorylation. These proximal events stimulate the PI3K?CAKT and MAPK?CERK (RAS-RAF-MEK-ERK) cascades, alongside Rho GTPases (RAC1, CDC42, RHOA). Downstream effectors include transcription factors AP-1 and NF-??B, and cytoskeletal linkers vinculin and paxillin, collectively regulating adhesion, migration, proliferation, and survival.
In the DLD-1 colorectal cancer model, loss of ITGB1 disrupts integrin-mediated attachment to extracellular matrix components, impairing cell migration, invasion, and survival signaling. This knockout phenotype mirrors aspects of metastatic attenuation observed when integrin function is compromised, allowing researchers to delineate ITGB1-dependent mechanisms that sustain tumor cell viability under detached conditions. The polyclonal composition better represents intratumoral heterogeneity, enhancing translational relevance for studying integrin pathway inhibition in colorectal adenocarcinoma.
Applications span cell adhesion assays on coated surfaces, Transwell migration and invasion studies, and drug sensitivity testing. Western blotting for phospho-FAK and phospho-ERK serves as a pathway activity readout, while flow cytometry verifies heterogeneous ITGB1 surface loss. Immunofluorescence for paxillin visualizes focal adhesion dynamics, and proliferation or apoptosis assays assess functional endpoints. This pooled knockout model is particularly suited for genetic screens and co-culture environments. For further information, please contact Ascent Research.
