IGSF8 Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Ca Ski cervical carcinoma cell line. This heterogeneous pool carries targeted disruption of the IGSF8 gene, eliminating functional IGSF8 protein expression. As a polyclonal knockout model, it avoids clonal selection bias and provides a realistic cellular context for studying IGSF8 loss in cervical cancer biology.
The Ca ski cell line is a well-established model of cervical squamous cell carcinoma, originally isolated from a metastasis and characterized by stable integration of high-risk human papillomavirus type 16 (HPV-16) DNA. These adherent epithelial cells express the viral E6 and E7 oncoproteins, which inactivate p53 and pRb tumor suppressors, respectively, and they retain the ability to form tight junctions, making them particularly suitable for investigating epithelial barrier function and cell adhesion.
IGSF8 (CD316) is an immunoglobulin superfamily transmembrane protein localized to epithelial tight junctions and cell?Ccell contacts. It is transcriptionally regulated by AP-1 and TGF-beta, and its expression is modulated by HPV-16 E6/E7. IGSF8 interacts directly with integrin beta1 (ITGB1) and tetraspanins such as CD81, linking to focal adhesion kinase (FAK) and Src kinase signaling. These complexes mediate downstream effects on tight junction components Claudin-1, Occludin, and ZO-1, ultimately activating PI3K/AKT pathways and influencing epithelial?Cmesenchymal transition (EMT) and cell migration.
Disruption of IGSF8 in Ca ski cells impairs tight junction integrity, enhances cell migration and invasion, and promotes EMT, mirroring aspects of cervical cancer progression. The HPV-16-positive background allows investigation of how viral oncoproteins synergize with IGSF8-dependent adhesion signaling to drive metastatic behavior and alter drug sensitivity. Thus, this knockout model serves as a valuable tool for dissecting the molecular mechanisms linking adhesion dysregulation to tumor aggressiveness and therapeutic resistance.
These cells are applied in tight junction studies using transepithelial electrical resistance (TEER) and immunofluorescence, migration and invasion assays (e.g., Boyden chamber), quantitative expression analysis of EMT markers by RT-qPCR and Western blotting, and phospho-specific detection of FAK and AKT activation. Additional uses include drug sensitivity profiling via viability and apoptosis assays, and exploration of IGSF8??s role in immune synapse modulation. For further information, please contact Ascent Research.
