The ICAM1 Knockout Ca Ski Polyclonal Cells are a polyclonal cell population generated from Ca Ski cervical squamous carcinoma cells through CRISPR/Cas9-mediated disruption of the ICAM1 gene, providing a heterogeneous knockout pool suitable for pooled functional assays. This knockout model offers a stable loss-of-function system for studying ICAM1-driven adhesion, signaling, and migration.
The Ca Ski parental line is derived from a cervical squamous cell carcinoma and harbors integrated, transcriptionally active HPV-16 genomes, constitutively expressing the E6 and E7 oncoproteins. It is a well-established model for HPV-16-positive cervical cancer, widely used to examine transformed epithelial cell interactions with immune effectors, and frequently employed in cervical cancer research and drug screening.
ICAM1 (CD54) is an inducible adhesion molecule that mediates leukocyte firm adhesion and transendothelial migration. Its expression is upregulated by TNF-??, IL-1??, and IFN-?? via NF-??B and AP-1. Ligation by LFA-1 or Mac-1 triggers RhoA activation, actin reorganization, and phosphorylation of ERM proteins and downstream paxillin/FAK signaling, facilitating leukocyte diapedesis. ICAM1 also serves as a receptor for rhinoviruses, coxsackievirus A21, and fibrinogen, highlighting its role in inflammation and host?Cpathogen interactions.
In Ca Ski cells, ICAM1 knockout enables dissection of how HPV transformation influences adhesion and immune cell interactions. Because these cells maintain cytokine-responsive NF-??B signaling, the model is suited for analyzing ICAM1 induction and downstream RhoA/ROCK-dependent cytoskeletal remodeling. The knockout also allows assessment of ICAM1??s role in HPV-positive tumor cell migration and potential involvement in metastatic dissemination. Furthermore, the model can be used to investigate ICAM1-dependent viral entry pathways.
Typical experiments include static and shear flow leukocyte adhesion assays, transwell migration and transmigration studies, and immunofluorescence microscopy of junctional proteins. The cells are compatible with NF-??B luciferase reporter assays, cytokine stimulation time-courses, and analysis of RhoA/ROCK pathway activation to explore ICAM1 transcriptional control and downstream signaling. They also support screening of anti-adhesion therapeutics and viral entry studies. Validation can be performed by flow cytometry, Western blotting, and RT-qPCR. For further information, contact Ascent Research.
