The ITGB3 Knockout AGS Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human gastric adenocarcinoma cell line AGS. This product features a pool of edited cells with heterogeneous ITGB3 gene disruptions, providing a robust loss-of-function model for studying integrin beta-3 biology without clonal selection. The polyclonal format preserves population-level heterogeneity, making it suitable for experiments where averaged knockout effects are desired across a genetically diverse background. This model is designed for researchers investigating ITGB3-dependent mechanisms in gastric epithelial cells.
The parental AGS cell line is a widely used human gastric adenocarcinoma epithelial model, originally isolated from a patient with poorly differentiated gastric carcinoma. It offers a physiologically relevant context for exploring the molecular underpinnings of gastric cancer pathology, including aberrant cell adhesion, migration, and survival signaling. AGS cells exhibit epithelial morphology and retain key signaling pathways commonly deregulated in gastric cancer, enabling direct assessment of gene function in a disease-relevant background without the need for exogenous pathway activation.
ITGB3 encodes integrin beta-3, a subunit that heterodimerizes with alpha-v (ITGAV) or alpha-IIb (ITGA2B) to form receptors for extracellular matrix proteins such as vitronectin, fibronectin, fibrinogen, and von Willebrand factor. Upon ligand binding, these integrins activate focal adhesion kinase (FAK) and Src, initiating cascades that include PI3K-Akt, MAPK (ERK1/2), and RhoA pathways. Key downstream effectors like paxillin, vinculin, and NF-??B mediate cell adhesion, migration, proliferation, and survival. The signaling network is further regulated by intracellular activators talin and kindlin, and interacts with adaptor proteins Shc and Grb2, linking extracellular cues to multiple oncogenic routes.
In the AGS gastric cancer model, ITGB3 knockout disrupts integrin-mediated adhesion and migration, processes frequently exploited by metastatic cancer cells. Loss of ITGB3 attenuates signaling through FAK-Src and PI3K-Akt, potentially reducing invasive capacity. Integrin beta-3 is also implicated in angiogenesis and platelet-tumor cell interactions, making this knockout model valuable for studying tumor progression and microenvironment crosstalk. Researchers can dissect the contribution of ITGB3 to oncogenic phenotypes in a gastric epithelial setting.
Researchers can employ this polyclonal knockout model in applications including cancer cell adhesion and migration studies, angiogenesis inhibition assays, integrin-targeted therapy screening, and drug resistance investigations. Representative experimental workflows include western blotting for ITGB3 and downstream signaling proteins (e.g., phosphorylated FAK, Akt, ERK1/2), cell adhesion assays on vitronectin- or fibronectin-coated surfaces, transwell migration/invasion assays, flow cytometry for surface integrin analysis, and immunofluorescence staining of focal adhesions. For further technical details, please contact Ascent Research.
