The ITGA10 Knockout SaOS-2 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human SaOS-2 osteosarcoma line, engineered for loss-of-function studies of the ITGA10 gene. This heterogeneous pool of cells harbors targeted disruptions in ITGA10, providing a robust model to investigate the functional consequences of integrin alpha10 deletion without clonal biases. The product is designed for population-level analysis, enabling researchers to study overall genotypic and phenotypic effects in a bone cancer context.
SaOS-2 is a widely utilized human osteosarcoma cell line established from an 11-year-old female, characterized by osteoblast-like properties including high alkaline phosphatase activity and osteoblastic differentiation capacity. This line serves as a relevant model for bone tumor biology, recapitulating features of osteosarcoma progression and metastasis. Its mesenchymal origin and expression of bone matrix proteins make it particularly suited for examining integrin-mediated adhesion and signaling in a skeletal tumor microenvironment.
ITGA10 encodes the integrin alpha10 subunit, which pairs with ITGB1 to form the alpha10beta1 collagen receptor. This heterodimer binds collagen types I, II, and IV, activating focal adhesion kinase (FAK) and SRC to phosphorylate downstream targets including paxillin, AKT, and ERK1/2. Upstream regulators such as TGF-beta, BMP-2, and mechanical strain modulate this signaling, which converges on Rho GTPases (Rac1, Cdc42) to control adhesion and migration. The receptor complex associates with talin, kindlin, and filamin A, linking the ECM to the actin cytoskeleton and promoting cell survival and motility via PI3K-AKT and MAPK/ERK pathways.
In osteosarcoma, alpha10beta1-mediated collagen adhesion may drive local invasion and metastatic dissemination. Knocking out ITGA10 in SaOS-2 cells likely impairs collagen-induced FAK/AKT activation, reducing migratory and invasive capacities, thus clarifying the integrin’s role in tumor progression. This model allows dissection of mechanotransduction and ECM-dependent signaling pathways critical for bone cancer pathology.
Representative assays include collagen adhesion and transwell migration tests, immunofluorescence for focal adhesion components (paxillin, vinculin), western blotting for phospho-FAK and phospho-ERK, flow cytometry for integrin surface expression, and phospho-kinase arrays. The polyclonal knockout pool is valuable for drug screening targeting integrin pathways, mechanobiology studies under physiological strain, and metastasis modeling. For further details, please contact Ascent Research.
