The ALB Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the human cervical carcinoma cell line Ca Ski. This product provides a heterogeneous pool of cells carrying targeted disruption of the ALB gene, which encodes serum albumin. The polyclonal format enables functional screening and phenotypic analysis without the bias of single-cell isolation, making it suitable for studying albumin??s roles in a physiologically relevant cancer-cell context. The knockout model eliminates endogenous albumin expression, providing a clean background for dissecting albumin-mediated processes.
The host Ca Ski cell line is derived from a metastatic cervical epidermoid carcinoma and is positive for human papillomavirus type 16 (HPV-16). It is widely employed as a model system for investigating HPV-driven oncogenesis, cervical cancer progression, and host?Cvirus interactions. Ca Ski cells retain characteristics of cervical epithelial tumors, including active HPV oncogene expression, which drives malignant transformation and contributes to altered cellular metabolism, proliferation, and stress responses.
Albumin is a major plasma protein with dual roles as a carrier and antioxidant. It binds and transports fatty acids, hormones, bilirubin, drugs, and metal ions, regulating their bioavailability. Albumin also scavenges reactive oxygen species, maintaining extracellular redox homeostasis. ALB expression is transcriptionally activated by liver-enriched factors HNF1A, HNF4A, and C/EBP proteins, and modulated by glucocorticoids and insulin. Downstream, albumin availability influences fatty acid transporter SLC27A1, intracellular binding protein FABP1, and nuclear receptor PPARG, which govern lipid metabolism and gene expression. Additionally, albumin interacts with neonatal Fc receptor (FcRn) and endocytic receptors megalin and cubilin, mediating cellular uptake of ligands. Disruption of ALB using CRISPR/Cas9 in Ca Ski cells perturbs these interconnected pathways, affecting nutrient import, hormone signaling, and oxidative stress responses.
In cervical carcinoma cells, particularly those harboring HPV-16, metabolic reprogramming and redox balance are critical for tumor maintenance and therapy resistance. Albumin??s role as a fatty acid shuttle and antioxidant may directly influence the proliferative and migratory capacity of Ca Ski cells. Knocking out ALB allows researchers to decouple extracellular carrier functions from cell-autonomous pathways, revealing how cancer cells adapt nutrient import, drug sensitivity, and oxidative defense in the absence of exogenous albumin. This model is particularly relevant for studying drug?Calbumin interactions that affect chemotherapeutic efficacy and for evaluating mechanisms of resistance in HPV-positive cervical cancers.
This polyclonal knockout cell population supports mechanistic and drug discovery studies. Researchers can examine fatty acid uptake (Nile Red), ROS levels, and proliferation/migration (MTT/Transwell), and perform drug sensitivity profiling to identify agents modulated by albumin. Molecular analyses include RT-qPCR, Western blotting, and ELISA for secreted albumin. By integrating these assays, the model enables investigation of albumin??s contribution to cancer cell metabolism, antioxidant defense, and host?Cvirus interactions in an HPV-16-positive cervical carcinoma setting. For ordering, technical specifications, and support, please contact Ascent Research.
