This product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from SK-HEP-1, with targeted disruption of the GOLGA7 gene. The polyclonal approach preserves genetic heterogeneity, making the model suitable for studying GOLGA7 loss-of-function in a more physiologically relevant context. As a versatile research tool, these cells enable investigation of Golgi-associated processes without the confounding effects of clonal selection.
SK-HEP-1 is a hepatic adenocarcinoma cell line established from ascites of a male patient, widely used in hepatocellular carcinoma (HCC) research. The cells exhibit both epithelial and endothelial-like features, enabling studies of tumor plasticity and angiogenesis. Their tumorigenic capacity and endothelial gene expression profile provide a unique system to examine crosstalk between cancer cells and the vascular microenvironment, and to evaluate contributions of the secretory pathway to HCC progression and metastasis.
GOLGA7 is a cis-Golgi golgin that tethers COPII vesicles, facilitating their fusion and maintaining Golgi stack organization. It is activated by RAB1 GTPase, ARF1, and GBF1, and interacts with GOLGA7B, GOLGB1, USO1, and the SEC23/24 coatomer complex. These interactions coordinate ER-to-Golgi transport of secretory cargo and cell surface receptors. Knockout of GOLGA7 disrupts this tethering mechanism, leading to impaired Golgi morphology and altered trafficking of proteins such as EGF-regulated receptors. Consequently, downstream signaling and secretion dynamics are perturbed, potentially affecting cell migration and tumorigenicity in SK-HEP-1 cells.
In SK-HEP-1 cells, GOLGA7 knockout provides insight into how Golgi dysfunction drives hepatocellular carcinoma. Disrupted ER-to-Golgi trafficking can alter secretion of angiogenic factors and matrix proteases, impacting the tumor microenvironment and metastatic dissemination. Given their endothelial-like properties, these cells are ideal for dissecting Golgi-dependent regulation of cell adhesion and transendothelial migration. This model also enables testing of compounds that target secretory pathway vulnerabilities in liver cancer, offering a relevant platform for drug discovery efforts.
These polyclonal knockout cells support a range of experimental applications. Golgi integrity can be visualized by immunofluorescence, and GOLGA7 ablation validated by Western blot. Secretion deficits are measurable via ELISA or VSV-G trafficking assays, while cell migration, invasion, and viability readouts characterize phenotypic outcomes. Transcriptomic analyses (RNA-seq, RT-qPCR for trafficking markers) reveal broader pathway alterations. The model is well-suited for drug screening against Golgi-dependent processes and for mechanistic studies into secretory control of cancer hallmarks. For further technical information, please contact Ascent Research.
