The ALB Knockout CAL-27 Polyclonal Cells are a polyclonal population of CAL-27 tongue squamous cell carcinoma cells engineered via CRISPR/Cas9 to disrupt the ALB gene, which encodes human serum albumin. This product provides a heterogeneous pool of knockout cells without clonal selection, ensuring a robust loss-of-function model that retains the genetic diversity of the parental line. The absence of albumin expression simplifies experimental interpretation in applications requiring an albumin-null background.
CAL-27, derived from a 56-year-old male with tongue squamous cell carcinoma, is a well-characterized epithelial cell line widely used in oral cancer research. These cells maintain key features of squamous carcinoma, including invasive and migratory properties, and are responsive to chemotherapeutic agents. Importantly, CAL-27 does not constitutively express albumin, making it an ideal host for studying potential ectopic albumin functions or for generating a clean knockout control for CRISPR screens.
ALB encodes albumin, a multifunctional serum protein that maintains oncotic pressure and serves as a carrier for hydrophobic ligands such as fatty acids, bilirubin, and various drugs. Albumin also displays antioxidant activity by scavenging free radicals and binding redox-active metal ions. Its expression is primarily regulated by liver-enriched transcription factors HNF1?? and C/EBP??, with additional modulation by glucocorticoids, insulin, and amino acid levels. Albumin interacts with multiple partners, including the cell-surface receptors albondin (gp60) and FcRn, which facilitate its transport and recycling. In this knockout model, disruption of ALB eliminates albumin-mediated ligand delivery and antioxidant effects, enabling investigation of these processes in a squamous carcinoma context.
Although traditionally considered a liver-specific product, emerging evidence suggests that albumin may be taken up by tumor cells or play a role in the tumor microenvironment. This ALB knockout in CAL-27 cells permits rigorous examination of albumin??s influence on squamous cell carcinoma proliferation, invasion, and drug response. The model also serves as an essential negative control for CRISPR-based functional genomics, eliminating potential confounding signals from albumin present in culture supplements or expressed at low levels. Additionally, it provides a defined system for studying albumin-dependent drug binding and cellular uptake kinetics.
Researchers can apply this model to assess the impact of albumin loss on cell behavior using proliferation, wound healing, and drug uptake assays, complemented by molecular analyses such as RT-qPCR, western blotting, and ELISA to confirm gene disruption and pathway changes. Immunofluorescence may be used to examine receptor localization or albumin interactions. The polyclonal nature of the product supports robust, reproducible results across a diverse genetic background. For technical details and ordering information, please contact Ascent Research.
