The AIFM2 Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell pool featuring targeted disruption of the AIFM2 gene in the human Ca Ski cervical carcinoma line. This heterogeneous population provides a robust loss-of-function model for studying AIFM2-dependent ferroptosis and redox biology without the need for clonal isolation. The polyclonal format preserves genetic diversity while ensuring consistent ablation of AIFM2 function across the culture.
The parental Ca Ski cell line originates from a metastatic human cervical epidermoid carcinoma and harbors an integrated HPV-16 genome, with characteristic epithelial morphology and expression of the viral E6 and E7 oncoproteins. These oncoproteins target critical tumor suppressors including TP53, establishing Ca Ski as a clinically relevant model for HPV-driven cervical cancer research, viral oncogenesis, and therapeutic response studies.
AIFM2, also designated ferroptosis suppressor protein 1 (FSP1), functions as a key inhibitor of ferroptosis by catalyzing the NAD(P)H-dependent reduction of coenzyme Q10 at the plasma membrane. This reaction generates ubiquinol, a radical-trapping antioxidant that directly blocks lipid peroxidation propagation, thereby preventing ferroptotic cell death. This activity is mechanistically distinct from AIFM2??s mitochondrial pro-apoptotic role. AIFM2 expression is regulated by transcription factors such as TP53, NFE2L2 (NRF2), and HIF1A, and the protein operates within a network that includes SLC7A11, GPX4, ACSL4, and lipoxygenases (ALOX), all of which collaboratively govern cellular sensitivity to lipid reactive oxygen species.
In the Ca Ski cervical carcinoma context, AIFM2 knockout eliminates a critical ferroptosis defense, offering a valuable system to examine how HPV oncoprotein activity may influence susceptibility to ferroptosis-inducing agents. This model facilitates investigation of redox balance perturbations and potential therapeutic strategies to overcome drug resistance by targeting the lipid antioxidant machinery in HPV-positive malignancies.
This polyclonal knockout cell pool is ideally suited for ferroptosis mechanism studies, cervical cancer biology, and drug resistance research. Representative assays include lipid peroxidation monitoring via C11-BODIPY staining, ferroptosis induction with erastin or RSL3, cell viability measurements, coenzyme Q10 quantification, Western blotting, RT-qPCR, immunofluorescence, and flow cytometry for lipid ROS detection. These applications enable dissection of AIFM2-dependent pathways and evaluation of ferroptosis-targeted interventions in a disease-relevant epithelial cell model. For additional information or technical inquiries, please contact Ascent Research.
