The CCN2 Knockout A2780 Polyclonal Cells product comprises an A2780 ovarian carcinoma population with CRISPR/Cas9-mediated disruption of the CCN2 gene, provided as a polyclonal knockout pool. This format retains genetic diversity while eliminating CCN2 expression, avoiding clonal selection biases and ensuring a more representative cellular background for functional studies. The cells are prepared for immediate use, offering a convenient and robust model for interrogating CCN2-dependent biology in a human epithelial ovarian cancer context.
A2780 is a human ovarian endometrioid adenocarcinoma cell line established from a primary tumor. It is extensively utilized as an in vitro model for epithelial ovarian cancer, enabling investigation of oncogenic signaling, tumor?Cstroma interactions, and chemoresistance mechanisms, particularly to platinum compounds. Its epithelial characteristics, tumorigenic capacity, and genetic tractability render it an ideal host for gene disruption studies focused on matricellular proteins and their roles in cancer progression.
CCN2 encodes connective tissue growth factor (CTGF), a matricellular protein that is induced by TGF-??, mechanical stress, hypoxia, angiotensin II, and endothelin-1. Secreted CCN2 interacts with cell surface integrins ??v??3 and ??5??1, as well as the endocytic receptor LRP1, and orchestrates signaling through SMAD2/3, ERK1/2, FAK, AKT, and YAP/TAZ pathways. These cascades culminate in the transcriptional upregulation of extracellular matrix components such as collagen I (COL1A1) and fibronectin (FN1), angiogenic factors like VEGFA, and matrix metalloproteinase 2 (MMP2). Through these effectors, CCN2 regulates cell adhesion, migration, proliferation, and ECM remodeling, processes central to fibrotic and neoplastic diseases.
In A2780 cells, CCN2 contributes to a pro-invasive phenotype by enhancing ECM deposition, focal adhesion dynamics, and paracrine signals that promote angiogenesis and desmoplasia. Knockout of CCN2 in this polyclonal population disrupts CTGF-mediated integrin signaling and attenuates the downstream activation of FAK, ERK, and YAP/TAZ, thereby impairing cell motility and matrix contraction. This model thus provides a powerful tool to dissect the molecular mechanisms by which CTGF drives ovarian cancer aggressiveness and stromal remodeling, and to test therapeutic strategies targeting the CTGF axis.
The CCN2 Knockout A2780 Polyclonal Cells are suitable for fibrosis mechanism studies, tumor microenvironment analysis, and extracellular matrix remodeling. Commonly employed assays include western blotting for CCN2 protein, RT-qPCR for mRNA quantification, cell migration and invasion assays, collagen gel contraction, immunofluorescence for ECM proteins, phospho-signaling analysis (p-SMAD2, p-ERK1/2), co-immunoprecipitation of integrin complexes, and RNA-seq. For further information, contact Ascent Research.
