The CCN2 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric adenocarcinoma cell line. This product provides a loss-of-function model for the CCN2 gene, which encodes the matricellular protein connective tissue growth factor (CTGF). The polyclonal pool format retains the genetic diversity of the original cell population, making it suitable for applications such as large-scale drug screening, signaling pathway analysis, and functional genomics studies where clonal homogeneity is not required.
The AGS cell line was originally isolated from a human gastric adenocarcinoma and has become a well-established model for gastric cancer research. These epithelial cells are routinely employed to investigate Helicobacter pylori infection, oncogenic signaling, and the epithelial-mesenchymal transition (EMT) that drives tumor invasion and metastasis. Their robust growth and thoroughly characterized signaling pathways make them an ideal host for gene knockout experiments focused on gastric carcinogenesis and tumor-stroma crosstalk.
CCN2 functions as a central mediator of TGF-??-induced fibrogenesis and EMT. Its expression is upregulated by TGF-??1, endothelin-1, angiotensin II, hypoxia (via HIF-1??), and mechanical stress. Secreted CTGF interacts with cell surface integrins (??v??3, ??5??1), LRP1, EGFR, and heparin sulfate proteoglycans, triggering intracellular signaling through FAK, ERK1/2, JNK, Akt, and YAP/TAZ. These pathways converge to promote the expression of collagen type I, fibronectin, MMP-2, MMP-9, and CTGF itself, thereby enhancing cell adhesion, migration, proliferation, and extracellular matrix deposition.
In AGS gastric cancer cells, disruption of CCN2 is expected to impair TGF-??-driven EMT and fibrotic responses, attenuating migratory and invasive capabilities. This polyclonal knockout population is therefore a powerful tool for dissecting CCN2-dependent mechanisms in gastric tumor progression and for exploring the interplay between TGF-?? and integrin signaling in the tumor microenvironment. Comparative studies using wild-type and knockout cells can elucidate the contribution of CCN2 to growth factor-induced phenotypic changes.
Researchers can employ these cells in a variety of assays, including western blotting for EMT markers (E-cadherin, vimentin), transwell migration and invasion assays, collagen gel contraction assays, RT-qPCR analysis of fibrotic gene expression, immunofluorescence staining for F-actin and focal adhesions, global transcriptomic profiling by RNA-seq, and phospho-SMAD analysis following TGF-?? stimulation. These applications support investigations into gastric cancer EMT, fibrosis, anti-fibrotic drug discovery, and tumor-stroma interactions. For additional information, please contact Ascent Research.
