The ITGB3 Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of human 143B osteosarcoma cells in which the ITGB3 gene has been disrupted, leading to loss of integrin ??3 protein expression. This knockout model provides a genetically defined system to study integrin ??3 functions without clonal selection bias, enabling robust loss-of-function analyses across a heterogeneous cell population.
The parental 143B line is a TP53-mutant osteosarcoma cell line widely used in cancer research to model bone tumor biology, including cell adhesion, migration, and metastasis. Its origin from a human bone cancer makes it a relevant host for dissecting integrin-mediated processes within the tumor microenvironment and bone matrix interactions.
ITGB3 encodes integrin ??3, a transmembrane subunit that heterodimerizes with ??V (ITGAV) or ??IIb (ITGA2B) to bind ECM ligands such as fibronectin, vitronectin, and fibrinogen. Ligand-bound integrins recruit talin and kindlin, triggering FAK and Src kinase activation, which propagate signals through PI3K?CAKT and MAPK (ERK1/2) pathways. Downstream, small GTPases RAC1, CDC42, and RHOA coordinate cytoskeletal remodeling, while transcriptional coactivators YAP1 and TAZ mediate gene expression changes. ITGB3 expression is regulated by TGFB1, VEGFA, EGF, and transcription factors SP1 and AP-1. Knockout of ITGB3 ablates these adhesive and signaling complexes, offering a clean background for mechanistic studies.
In the 143B osteosarcoma background, ITGB3 contributes to integrin-dependent adhesion, migration, and survival signaling. Disruption of ITGB3 is expected to impair focal adhesion formation and reduce FAK autophosphorylation, thereby attenuating downstream pro-migratory and pro-survival pathways. This polyclonal knockout model allows researchers to evaluate the collective impact of ITGB3 loss on tumor cell behavior, reflecting the heterogeneity of osteosarcoma populations. It is particularly useful for investigating mechanisms of bone cancer metastasis and for testing inhibitors targeting integrin signaling.
These cells are suitable for functional assays such as cell adhesion on ECM substrates, Boyden chamber invasion, wound healing, and proliferation measurements. Standard characterization includes Western blotting for ITGB3 and key signaling molecules, phospho-FAK immunoblotting, immunofluorescence staining of focal adhesions, and flow cytometry for surface integrin expression. Co-immunoprecipitation can assess integrin complex integrity. Researchers exploring Glanzmann thrombasthenia or thrombosis may also exploit this model to examine platelet-independent ITGB3 functions. For technical support, please contact Ascent Research.
