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C3A is a clonal derivative of the human hepatoma line HepG2 selected for strong contact inhibition, high albumin production, and high AFP production; as cultures reach confluence, AFP secretion decreases while albumin increases. It is widely used as a human hepatocyte-like model for liver function and toxicity studies, including 3D spheroid systems that can improve liver-specific functions and toxicological predictivity compared with 2D culture. C3A exhibits nitrogen metabolism comparable to perfused rat liver and shows oxygen-dependent gluconeogenesis activity. As a cancer-derived line, it serves as a model for HCC molecular subtypes (HepG2/C3A aligns with AFP-high/stemness-like profiles) and is used to study antiviral innate responses; for example, upon hepatitis E virus RNA replication, C3A upregulates pattern-recognition receptor genes (RIG-I, MDA5, TLR3) and supports lower HEV replication than certain Huh7 derivatives. C3A is a model system, not a single therapeutic target or receptor.
Not applicable as a drug target. In this context, drugs are used to probe hepatotoxic mechanisms (e.g., mitochondrial toxicity, reactive metabolite formation) in C3A assays rather than to act “on” C3A as a specific molecular target.
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