The CCN2 Knockout 769-P Polyclonal Cells are a polyclonal population of human 769-P renal cell carcinoma epithelial cells in which the CCN2 gene has been disrupted by CRISPR/Cas9 genome editing. This product provides a heterogeneous loss-of-function model that preserves the cellular diversity of the parental line while eliminating functional CCN2 expression, making it well-suited for investigating CTGF/CCN2-dependent mechanisms in cancer and fibrotic signaling.
The 769-P cell line was established from a primary clear cell renal cell carcinoma and is extensively used in kidney cancer research. These epithelial cells retain responsiveness to TGF-?? and can undergo epithelial?Cmesenchymal transition, offering a clinically relevant background for studying genes involved in renal tumor progression, extracellular matrix remodeling, and metastasis.
CCN2 encodes connective tissue growth factor (CTGF), a matricellular protein that regulates adhesion, migration, proliferation, and ECM production. CTGF is transcriptionally activated by TGFB1 via SMAD3/SMAD4 and is additionally regulated by HIF1A, angiotensin II, endothelin-1, and mechanical stress. It interacts with integrins ITGAV/ITGB3 and ITGA6/ITGB1, fibronectin, and perlecan to propagate signals through FAK, SRC, AKT1, and MAPK1/3. CTGF also induces expression of COL1A1, FN1, MMP2, and VEGFA, and binds CYR61, BMP4, and LRP1, integrating multiple pathways including Hippo/YAP/TAZ and Wnt.
In 769-P cells, CCN2 knockout disrupts TGF-?¨Cdriven profibrotic and protumorigenic responses. Loss of CTGF attenuates integrin-mediated adhesion signaling, reducing phosphorylation of FAK, Src, ERK1/2, and AKT, and dampening matrix protein and protease expression. These polyclonal knockout cells therefore serve as a powerful model to dissect CTGF??s role in renal tumor invasion, EMT, and microenvironment modulation, with polyclonality enhancing the translational relevance of findings.
Typical applications include Western blotting for CTGF and downstream effectors (phospho-FAK, phospho-ERK, phospho-AKT), RT-qPCR for CCN2, COL1A1, FN1, and MMP2, transwell migration/invasion assays, adhesion assays, immunofluorescence for focal adhesions, RNA-seq, TGF-?? stimulation, and co-immunoprecipitation with integrins. These approaches enable functional studies of CTGF in renal carcinoma, inhibitor screening, and signaling pathway validation. For further information, please contact Ascent Research.
