The CCN2 Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited population of human 143B osteosarcoma cells harboring targeted disruption of the CCN2 gene. This polyclonal knockout pool provides a heterogeneous loss-of-function model that bypasses clonal selection, enabling robust investigation of CCN2-mediated cellular processes in a malignant bone tumor background.
The 143B cell line is a widely utilized model of human osteosarcoma characterized by high metastatic potential and aggressive tumorigenicity. 143B cells form osteolytic lesions and exhibit pronounced migratory and invasive properties, making this background particularly relevant for studying tumor dissemination, extracellular matrix (ECM) remodeling, and bone microenvironment interactions.
CCN2 (CTGF) encodes a matricellular protein that regulates cell adhesion, migration, proliferation, and ECM synthesis. Acting as a downstream effector of TGF-beta, CCN2 is transcriptionally activated via SMAD2/3 and by factors including BMP2, BMP4, hypoxia, and mechanical stress. It interacts with integrin alphaVbeta3 and LRP1 to promote production of collagen type I (COL1A1, COL1A2) and fibronectin, while also upregulating MMP2 and VEGF. CCN2 signaling engages ERK1/2, FAK, AKT, and RhoA pathways, linking TGF-beta receptor activation to cytoskeletal remodeling and gene expression essential for matrix deposition and adhesion.
In 143B cells, CCN2 knockout impairs ECM synthesis, attenuates integrin-mediated adhesion, and reduces migratory and invasive capacity. Disruption of CCN2 interrupts TGF-beta-driven autocrine loops and dampens signaling through FAK, ERK1/2, and RhoA, thereby diminishing the malignant phenotype. This knockout model provides a valuable tool to elucidate the molecular underpinnings of osteosarcoma progression and the tumor-supportive ECM niche.
This product supports diverse applications in cancer metastasis, bone tumor biology, fibrosis, and ECM research. Assays such as western blotting for CTGF, RT-qPCR for collagen and fibronectin, transwell migration/invasion assays, cell adhesion assays, and immunofluorescence for matrix proteins are readily employed. Phospho-SMAD2/3 analysis can further probe TGF-beta pathway status. For further information or to discuss custom models, please contact Ascent Research.
