This product presents a CRISPR/Cas9-edited polyclonal knockout cell population targeting the EGFR gene in the human cervical cancer cell line Ca Ski. The polyclonal format consists of a heterogeneous mixture of cells harboring diverse gene disruptions, providing a robust loss-of-function model without clonal selection. This approach enables researchers to investigate EGFR-dependent phenotypes while averaging out clonal artifacts, making it suitable for population-level assays.
The Ca Ski cell line is derived from a cervical epidermoid carcinoma and harbors an integrated human papillomavirus type 16 (HPV-16) genome. As a widely used model for cervical cancer, Ca Ski cells retain key features of HPV-driven malignancy, including expression of viral oncoproteins E6 and E7, which interfere with tumor suppressors p53 and pRb. This genetic background offers a relevant platform to examine the interplay between EGFR signaling and HPV-mediated oncogenesis.
EGFR (epidermal growth factor receptor) is a receptor tyrosine kinase that plays a central role in cell proliferation, survival, and differentiation. Upon binding of ligands such as EGF, TGF-??, HB-EGF, amphiregulin, betacellulin, and epiregulin, EGFR undergoes dimerization and autophosphorylation, recruiting adaptor proteins including GRB2, SHC, and GAB1. This triggers downstream signaling through the GRB2-SOS-RAS-RAF-MEK-ERK cascade, the PI3K-AKT-mTOR axis, the JAK-STAT pathway, and PLC??-PKC signaling. EGFR also interacts with other ErbB family members (ErbB2, ErbB3, ErbB4) and regulatory proteins such as CBL and PTPN11 (SHP2), which modulate signal duration and intensity.
In Ca Ski cells, EGFR signaling contributes to oncogenic phenotypes including enhanced proliferation and migration. The presence of HPV-16 oncoproteins may influence EGFR activity and downstream effectors, creating a unique signaling context. Disruption of EGFR in this polyclonal model allows dissection of its specific contributions within a cervical cancer background, enabling studies on how viral oncoproteins intersect with receptor tyrosine kinase networks and impact tumorigenesis.
This EGFR knockout polyclonal cell product is optimized for a range of functional analyses. Researchers can assess EGFR-dependent signaling by western blotting for total and phosphorylated EGFR, ERK (p-ERK), and AKT (p-AKT), or quantify EGFR transcript levels via RT-qPCR. Cell proliferation can be measured using MTT assays, while transwell migration and invasion assays evaluate motility changes. Drug sensitivity profiling with EGFR inhibitors such as gefitinib or erlotinib provides insights into therapeutic responses. For additional details or custom requests, please contact Ascent Research.
