The CCDC82 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited human liver adenocarcinoma cell population with targeted disruption of the CCDC82 gene. This polyclonal knockout model provides a heterogeneous loss-of-function system for studying the tumor-suppressive roles of coiled-coil domain-containing protein 82 in hepatocellular carcinoma. The product comprises a pool of edited cells harboring diverse gene-disruption events, enabling robust analysis of gene function without clonal bias.
The parental SK-HEP-1 cell line originates from ascitic fluid of a male patient with liver adenocarcinoma. It is widely employed as an in vitro model for hepatocellular carcinoma, faithfully recapitulating key features of liver cancer biology including dysregulated signaling, anchorage-independent growth, and metastatic potential. SK-HEP-1 cells are characterized by epithelial morphology and are amenable to standard cell culture and transfection protocols, making them a versatile host for genetic perturbation studies.
CCDC82 encodes a coiled-coil domain protein that functions as a putative tumor suppressor by directly interacting with ??-catenin (CTNNB1) and facilitating its ubiquitin-proteasome-mediated degradation. This interaction is mediated in part by the E3 ubiquitin ligase complex components BTRC and SKP1. Consequently, CCDC82 negatively regulates the Wnt/??-catenin signaling pathway, where it suppresses the transcriptional activity of TCF/LEF factors and dampens expression of oncogenic targets such as MYC and CCND1. Upstream, CCDC82 expression is subject to epigenetic silencing by promoter methylation through DNMTs and histone deacetylases (HDACs), as well as transcriptional regulation by tumor suppressors including TP53 and the FOS/JUN complex. The protein also influences cytoskeletal dynamics via interactions with actin and tubulin and modulates Rho GTPase activity.
In the context of SK-HEP-1 hepatocellular carcinoma cells, knockout of CCDC82 relieves the inhibition on Wnt/??-catenin signaling, leading to stabilization of ??-catenin, its nuclear accumulation, and persistent activation of Wnt target genes. This molecular shift drives a more aggressive phenotype characterized by increased cell proliferation, enhanced migration, and reduced apoptosis??hallmarks of liver adenocarcinoma progression. Thus, this knockout model recapitulates a clinically relevant loss-of-tumor-suppressor function and provides a powerful platform for interrogating the role of CCDC82 in liver cancer pathogenesis and metastasis.
This polyclonal knockout product is ideally suited for a broad range of research applications. Investigators can employ it to dissect CCDC82-dependent tumor suppressor mechanisms using co-immunoprecipitation, ubiquitination assays, and ??-catenin localization studies. Functional assays such as CCK-8, EdU proliferation assays, Transwell migration, wound healing, and flow cytometric analysis of cell cycle and apoptosis enable quantitative phenotypic assessment. Furthermore, the model is valuable for drug screening campaigns targeting the Wnt pathway, for instance, testing inhibitors like XAV939 and IWP-2, and for exploring epigenetic reactivation of CCDC82. For further information, please contact Ascent Research.
