CCDC93 Knockout Huh-7 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated by disrupting the CCDC93 gene in the Huh-7 host cell line. This mixed population of edited cells provides a loss-of-function model for investigating endosomal trafficking and receptor signaling in hepatocellular carcinoma without the biases of clonal selection.
Huh-7 is a well-differentiated hepatocellular carcinoma cell line derived from a liver tumor of a 57-year-old Japanese male. These epithelial cells retain hepatocyte characteristics and serve as a widely used model for studying liver cancer, hepatic metabolism, and cellular proliferation.
CCDC93 is a core component of the CCC complex, which partners with the retromer (VPS35, VPS26, VPS29) and WASH complexes to orchestrate endosomal recycling of surface receptors. It directly binds CCDC22 and COMMD1-10, and associates with SNX27 to sort cargoes such as EGFR, Notch1, and the copper transporter ATP7A. Upstream activation by EGF, Notch ligands, and Rab7 promotes complex formation, while downstream consequences of CCDC93 loss include elevated NF-??B activity, impaired Notch degradation, and disrupted copper homeostasis.
This knockout model in Huh-7 hepatocellular carcinoma cells enables dissection of how endosomal trafficking defects fuel oncogenic signaling. The loss of CCDC93 perturbs recycling of key receptors, leading to sustained NF-??B activation, aberrant Notch signaling, and altered copper distribution that may promote tumor growth, inflammation, and resistance to therapy.
Applications include mechanistic studies of endosomal sorting in liver cancer, investigation of Notch and NF-??B crosstalk, analysis of copper metabolism, and drug sensitivity screening with agents like sorafenib or cisplatin. Assays such as Western blotting, co-immunoprecipitation, immunofluorescence, flow cytometry, and luciferase reporters can be employed. For further details, please contact Ascent Research.
