CCN2 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the CAL-27 human oral squamous cell carcinoma cell line, designed for functional studies of connective tissue growth factor (CTGF). The product offers a pooled loss-of-function model in which CCN2 gene disruption is introduced by CRISPR/Cas9-mediated genome editing, enabling investigation of CCN2-dependent signaling in a relevant epithelial tumor context.
CAL-27 is an established epithelial cell line derived from a human tongue squamous cell carcinoma, widely employed as an in vitro model for studying oral squamous cell carcinoma (OSCC) biology, including tumor cell proliferation, invasion, and response to therapeutic agents. The cells exhibit characteristic features of aggressive oral tumors and provide a reproducible host system for dissecting molecular mechanisms of OSCC progression.
CCN2 encodes connective tissue growth factor (CTGF), a secreted matricellular protein that functions as a key mediator of fibrogenic and tumorigenic signaling. CTGF is transcriptionally upregulated by TGF-beta via SMAD2/3 and ETS-1, as well as by hypoxia and mechanical stress, and interacts with integrins ??V??3 and ??5??1, LRP1, LRP6, and heparin. Downstream, CTGF promotes expression of extracellular matrix components such as COL1A1, COL1A2, and fibronectin (FN1), matrix metalloproteinases MMP2 and MMP9, and vascular endothelial growth factor (VEGF). In the context of CAL-27 cells, CCN2 knockout disrupts TGF-beta-induced signaling through SMAD2/3 and integrin-mediated FAK/Src/p38 MAPK cascades, impairing matrix synthesis, adhesion, and cytoskeletal reorganization.
In oral squamous cell carcinoma, CTGF is frequently overexpressed and contributes to tumor progression by enhancing extracellular matrix remodeling, promoting epithelial-mesenchymal transition (EMT), and facilitating metastatic dissemination. The CCN2 Knockout CAL-27 Polyclonal Cells enable dissection of CTGF-dependent pathways in a clinically relevant OSCC model, providing a platform to study tumor cell-autonomous and paracrine effects of CTGF secretion. This model is particularly suited for examining how loss of CCN2 affects cell proliferation, migration, invasion, and adhesion to matrix proteins, as well as for evaluating the interplay between CTGF and integrin signaling in the tumor microenvironment.
Typical applications include functional characterization of CCN2 in OSCC, investigation of TGF-beta-induced EMT, drug screening for anti-fibrotic or anti-metastatic agents, and co-culture models to analyze tumor-stroma interactions. The cells can be used in Transwell migration and invasion assays, cell proliferation and apoptosis assays, and Western blotting to monitor CTGF expression and downstream effectors such as phospho-SMAD2/3, integrin ??V??3, and fibronectin. RNA-seq or RT-qPCR can assess transcriptional changes, while immunofluorescence and collagen gel contraction assays enable evaluation of matrix remodeling. These polyclonal knockout cells also support xenograft tumor studies to examine in vivo tumor growth and metastasis. For further technical details or custom requirements, please contact Ascent Research.
