The CCDC91 Knockout SK-HEP-1 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human SK-HEP-1 cell line, featuring targeted disruption of the CCDC91 gene. This polyclonal knockout model provides a loss-of-function system for investigating the role of CCDC91 in maintaining Golgi apparatus organization and intracellular trafficking pathways. The cells are supplied as a heterogeneous population harboring a range of gene-editing events, offering a robust tool for functional studies without clonal selection artifacts, and are suitable for applications in hepatocellular carcinoma research, membrane trafficking analysis, and drug discovery.
The SK-HEP-1 host cell line is a hepatic adenocarcinoma epithelial cell type originally established from the ascites of a patient with liver adenocarcinoma. As a widely used model in liver cancer research, SK-HEP-1 cells retain key characteristics of tumorigenic hepatocytes, including migratory and invasive properties relevant to metastasis studies. Their endothelial-like phenotypic features and ability to form tumors in xenograft models make them particularly valuable for examining the interplay between intracellular transport and malignant behavior in hepatocellular carcinoma.
CCDC91 localizes to the Golgi apparatus and functions as a structural organizer essential for Golgi stack integrity and efficient vesicle-mediated trafficking. It interacts directly with core Golgi matrix proteins, including GM130 (GOLGA2) and golgin-160 (GOLGB1), and associates with microtubule-associated proteins to coordinate vesicle tethering and cargo processing. Through these interactions, CCDC91 regulates the transport of downstream targets such as Golgi-resident glycosylation enzymes, cell surface receptors, and secretory proteins. Disruption of CCDC91 expression leads to fragmentation of the Golgi ribbon, altered glycosylation patterns, and impaired secretion, ultimately affecting receptor presentation and downstream signaling cascades.
In the SK-HEP-1 hepatic adenocarcinoma context, loss of CCDC91 disrupts Golgi-dependent pathways that are frequently dysregulated in hepatocellular carcinoma. The resulting changes in protein trafficking can modify the cell surface proteome, influence cell?Ccell and cell?Cmatrix interactions, and alter secretory profiles. These effects may contribute to altered tumor cell proliferation, survival, and metastatic dissemination. This polyclonal knockout model thus offers a physiologically relevant platform to dissect how Golgi dysfunction reshapes the oncogenic properties of liver cancer cells.
This knockout cell model is engineered for a diverse range of research applications, including Western blotting for GM130 to monitor Golgi integrity, immunofluorescence microscopy to visualize Golgi morphology, flow cytometry to quantify surface receptor abundance, secretion assays (e.g., albumin or cytokine secretion) to assess trafficking efficiency, and migration/invasion assays to evaluate metastatic potential. It is ideally suited for mechanistic studies of Golgi biology in hepatocellular carcinoma, screening of Golgi-targeted therapeutic agents, and exploration of signaling networks dependent on proper vesicular transport. For technical inquiries or further product details, please contact Ascent Research.
