The CCDC167 Knockout Huh-7 Polyclonal Cells consist of a polyclonal Huh-7 population with CRISPR/Cas9-mediated disruption of the CCDC167 gene, offering a loss-of-function model to study coiled-coil domain-containing protein 167 in hepatocellular carcinoma (HCC). These polyclonal knockout cells retain the parental Huh-7 characteristics, including adherent epithelial morphology and permissiveness to hepatitis C virus replication, while capturing diverse editing events suitable for phenotypic screening and functional genomics.
Originating from a 57-year-old male with well-differentiated HCC, Huh-7 cells are a standard model in liver cancer research due to their reproducible tumorigenic properties and utility in antiviral studies. The adherent, epithelial line supports hepatitis C virus replication, facilitating viral pathogenesis and drug testing. Introducing a CCDC167 knockout into this system enables direct examination of gene function in hepatocarcinogenesis and tumor maintenance.
CCDC167 contains coiled-coil domains that mediate protein?Cprotein interactions, potentially linking it to cytoskeletal components like actin and tubulin and to small GTPases (Rho, Rac) in pathways controlling proliferation and cytoskeletal remodeling. Upstream regulation may involve HNF4A or MYC, transcription factors commonly affected in liver cancer. CCDC167 may also participate in ciliogenesis. Disruption of CCDC167 allows dissection of its roles in protein complex formation and cytoskeletal dynamics.
In HCC, dysregulated cytoskeletal organization and unchecked proliferation drive tumor aggression. CCDC167 knockout in Huh-7 cells provides a platform to assess impacts on cell growth, colony formation, motility, and invasion??key metastatic traits. The model supports drug sensitivity profiling to identify therapies whose effectiveness depends on CCDC167 status, offering insights for precision oncology. Since CCDC167 alterations occur in some liver cancers, this tool helps elucidate its contribution to malignancy.
Applications include gene expression analysis by RT?qPCR, protein detection via Western blot and immunofluorescence, and functional assays such as MTT, colony formation, and Transwell migration/invasion. Co?immunoprecipitation identifies interacting partners, while RNA?seq reveals dysregulated pathways. Xenograft tumor assays evaluate in vivo tumorigenicity. For more information, contact Ascent Research.
