The ITGB3 Knockout DLD-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of DLD-1 human colorectal adenocarcinoma cells, engineered to disrupt the ITGB3 gene. This polyclonal format provides a heterogeneous pool of knockout alleles, enabling robust loss-of-function studies without the limitations of single-cell clones. The cells serve as a powerful tool to investigate the roles of integrin beta-3 in adhesion, migration, and signaling within a colorectal cancer background.
The parental DLD-1 cell line is derived from a Dukes’ type C colorectal adenocarcinoma and exhibits epithelial morphology. It harbors oncogenic mutations in KRAS, PIK3CA, and TP53, making it a well-established model for advanced colorectal cancer. This genetic context is particularly relevant for studying tumor progression, metastasis, and drug resistance mechanisms, especially those intersecting with integrin-mediated pathways.
ITGB3 encodes integrin subunit beta-3, which heterodimerizes with alpha-v (ITGAV) or alpha-IIb (ITGA2B) to form receptors for vitronectin, fibronectin, and fibrinogen. Upon ligand binding, these integrins trigger outside-in signaling through FAK and Src, leading to activation of PI3K-Akt and MAPK/ERK cascades. Upstream regulators such as TGF-beta and VEGF modulate ITGB3 expression, while intracellular adaptors talin and kindlin control integrin activation. Downstream effectors include Rho GTPases, MMP2, MMP9, and anti-apoptotic factors like Bcl-2, collectively coordinating cell adhesion, spreading, migration, and survival.
In the DLD-1 colorectal cancer model, ITGB3-driven signaling promotes metastatic behaviors including enhanced migration, invasion, and resistance to anoikis. The knockout of ITGB3 in this polyclonal population abrogates beta-3 integrin function, enabling researchers to dissect its contributions to tumor cell adhesion on vitronectin, ECM remodeling, and pro-angiogenic signaling. This model is valuable for elucidating how beta-3 integrins cooperate with oncogenic KRAS and PI3K pathways to drive colorectal cancer progression.
These polyclonal knockout cells are suitable for a wide range of functional assays, including adhesion assays on vitronectin-coated plates, transwell migration and invasion assays, anoikis apoptosis analysis, and phospho-signaling profiling of FAK, Akt, and ERK. They can be employed in anti-metastatic and anti-angiogenic drug screening, studies of integrin crosstalk within the tumor microenvironment, and modeling of ITGB3-related disorders such as Glanzmann thrombasthenia. For further information or customized solutions, please contact Ascent Research.
