The CCN2 Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Ca Ski cervical carcinoma cell line, featuring targeted disruption of the CCN2 gene. This polyclonal pool offers a heterogeneous loss-of-function model that avoids clonal bias, enabling robust functional studies. The knockout cells are suited for diverse assays to dissect CCN2-dependent mechanisms in cancer and fibrosis.
The Ca Ski host cell line was established from a cervical epidermoid carcinoma metastasis and is widely used as a cervical cancer model. These epithelial cells are positive for human papillomavirus types 16 and 18, reflecting the viral etiology of cervical carcinogenesis. They retain signaling pathways critical for tumor progression, invasion, and extracellular matrix remodeling, providing a relevant context for examining CCN2 function.
CCN2 (CTGF) is a secreted matricellular protein that governs cell-matrix and cell-cell interactions. Activated by upstream stimuli such as TGF-??1, mechanical stress, hypoxia (HIF-1??), and angiotensin II, CCN2 binds integrins (??v??3, ??5??1) and co-receptors like LRP1 to trigger FAK and ERK1/2 kinase cascades. This signaling drives expression of fibrotic effectors including COL1A1, FN1, and MMP2, and promotes epithelial-mesenchymal transition through SMAD2/3, YAP/TAZ, and ??-catenin pathways, with CCN2 autoinduction reinforcing the response.
In the Ca Ski cervical carcinoma background, CCN2 knockout enables dissection of its contributions to tumor-stroma interactions, invasion, and metastatic progression. HPV-driven cancers frequently exhibit dysregulated TGF-?? signaling and ECM remodeling, processes in which CCN2 participates. Disrupting CCN2 allows researchers to assess its role in fostering a pro-fibrotic and pro-metastatic microenvironment, as well as its involvement in therapy resistance linked to integrin-mediated adhesion and downstream kinase activation.
This knockout population supports studies on fibrosis mechanisms, myofibroblast differentiation, and cancer cell plasticity. Representative assays include RT-qPCR and western blotting for CCN2 and ECM markers, phospho-signaling analysis (FAK, ERK), cell migration/invasion assays, immunofluorescence for collagen deposition, RNA-seq transcriptomics, and luciferase-based TGF-??/SMAD reporter assays. Applications extend to anti-fibrotic drug screening and target validation in cervical carcinoma. For further technical information, please contact Ascent Research.
