The HNF4A Knockout CAL-27 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal population with disruption of the HNF4A gene in the CAL-27 tongue squamous cell carcinoma line. This polyclonal knockout model provides a heterogeneous loss-of-function tool without the constraints of clonal selection, offering a physiologically relevant system for studying HNF4A-dependent pathways in cancer biology. The pooled format preserves genetic diversity, making it suitable for applications such as drug screening and transcriptional profiling.
CAL-27 is an epithelial cell line established from a 56-year-old male with tongue squamous cell carcinoma. As a well-characterized oral cancer model, it retains tumorigenic properties and is employed extensively in head and neck cancer research to examine invasion, metastasis, and therapeutics. The epithelial origin and active signaling networks of CAL-27 provide a pertinent context for investigating how HNF4A contributes to malignant phenotypes.
HNF4A is a nuclear receptor transcription factor central to the hepatocyte nuclear factor network, regulating epithelial differentiation, metabolism, and hepatocyte function. It is activated by HNF1A, HNF1B, AMPK, PPARGC1A, and retinoic acid, and transactivates targets including CYP3A4, APOB, SLC2A2, TTR, ALB, and UGT2B7. HNF4A interacts with coactivators MED1, NCOA6, and PPARGC1A, homodimerizes, and is inhibited by NR0B2, thereby coordinating glucose and lipid metabolism, drug processing, and epithelial identity.
In CAL-27 oral cancer cells, HNF4A knockout dismantles transcriptional programs governing epithelial differentiation and metabolic control, enabling the study of its potential tumor-suppressive or oncogenic functions. The loss of HNF4A attenuates expression of drug-metabolizing enzymes and nutrient transporters, which may alter chemosensitivity and metabolic fitness. This model allows investigation of how HNF4A deficiency impacts cancer cell behavior, including epithelial-mesenchymal transition and resistance to therapeutics.
Typical applications include mapping HNF4A target genes using ChIP-qPCR and RNA-seq, assessing functional outcomes with migration, invasion, and metabolic assays, and conducting drug sensitivity screens to link HNF4A status to compound efficacy. Standard validation by western blotting, RT-qPCR, flow cytometry, and immunofluorescence confirms knockout efficiency and downstream pathway perturbations. This polyclonal knockout pool supports both mechanistic exploration and translational research in oral squamous cell carcinoma. For technical inquiries, please contact Ascent Research.
