The AAMDC Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from SK-HEP-1 human liver adenocarcinoma cells, engineered for targeted disruption of the AAMDC gene. AAMDC encodes an adipogenesis-associated protein involved in lipid metabolism and adipocyte differentiation. The polyclonal format consists of a heterogeneous pool carrying diverse CRISPR-induced mutations, minimizing clonal selection biases and providing a robust loss-of-function model for pooled experimental strategies. This product is supplied as live cells intended for assays requiring abrogation of endogenous AAMDC function without single-clone isolation.
SK-HEP-1 is a widely used human hepatocellular carcinoma cell line isolated from ascitic fluid of a patient with liver adenocarcinoma. The cells exhibit an epithelial, tumorigenic phenotype and are extensively employed in research on hepatic malignancy, cancer metabolism, and drug responsiveness. Although classified as a liver adenocarcinoma line, SK-HEP-1 displays molecular features of endothelial and mesenchymal origins, offering a versatile platform for investigating pathways linking hepatocarcinogenesis and metabolic reprogramming. Its robust proliferation and amenability to standard transfection and CRISPR protocols facilitate generation of gene-edited variants for functional studies.
AAMDC is a key adipogenic factor governing lipid accumulation, operating in a transcriptional circuit controlled by PPARG and CEBPA, which serve as both upstream regulators and downstream targets, forming a feed-forward loop that amplifies adipogenic signaling. It modulates downstream effectors FABP4 and PLIN1 essential for lipid droplet biogenesis, while other pathway components, including ADIPOQ, SCD1, and FASN, regulate adipokine signaling and de novo lipogenesis. CRISPR/Cas9-mediated disruption of AAMDC is predicted to impair this network, resulting in attenuated lipid accumulation and impaired differentiation, exposing its role in metabolic homeostasis.
The intersection of adipogenic pathways and hepatocellular carcinoma metabolism is increasingly recognized as a driver of tumor progression. SK-HEP-1 cells retain adipogenic potential under specific stimuli, making them a relevant system to explore AAMDC’s contribution to lipid-driven liver cancer phenotypes. The gene’s links to adiposis dolorosa and lipomatosis underscore its clinical relevance. The polyclonal knockout population captures a spectrum of functional perturbations, enabling robust assessment of pathway dependencies and identification of AAMDC-dependent metabolic vulnerabilities in liver cancer cells.
Applications include adipogenesis assays with Oil Red O staining, gene expression analysis by RT?qPCR and Western blotting, and genomic validation by Sanger sequencing. Functional studies may utilize cell proliferation assays and RNA-seq transcriptomic profiling to define AAMDC-dependent gene networks. The model is well-suited for cancer metabolism research, studies of adipogenic signaling in liver cancer, and high-throughput screens where the polyclonal format enhances statistical reliability and reduces clonal artifacts. For further technical information, please contact Ascent Research.
