The CCDC93 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the CCDC93 gene has been disrupted in the SK-HEP-1 human liver adenocarcinoma cell line. This loss-of-function model enables detailed investigation of CCDC93-dependent processes. The polyclonal format provides a heterogeneous mix of edited alleles, reflecting population-level gene disruption for studying endosomal recycling and related cellular functions.
SK-HEP-1 is a hepatic epithelial cell line derived from ascites fluid of a hepatocellular carcinoma patient. It is widely used for liver cancer research, including tumor cell migration, invasion, and therapeutic testing, due to its adherent growth and stable phenotype. Introducing CCDC93 knockout into this background allows targeted interrogation of gene function in a disease-relevant hepatic context.
CCDC93 is a core subunit of the CCC (COMMD/CCDC22/CCDC93) complex that, together with retriever and retromer, mediates endosomal recycling of cell surface receptors. Key cargoes include integrins (ITGA5, ITGB1) and EGFR, whose plasma membrane return is critical for adhesion, migration, and proliferation. This recycling is triggered by upstream signals such as integrin engagement, EGF stimulation, and hypoxia, and requires interactions with CCDC22, COMMD1-10, VPS35L, and SNX17. CCDC93 also influences copper homeostasis through ATP7A trafficking. Downstream, the pathway engages the WASH complex, Rab5, Rab11, and NF-??B signaling, linking CCDC93 to integrin function and metal regulation.
In SK-HEP-1 cells, CCDC93 disruption presumably impairs integrin and EGFR recycling, disrupting adhesion, directional migration, and pro-metastatic signaling. Given the line’s metastatic origin, it is well-suited for studying how endosomal sorting defects drive hepatocellular carcinoma metastasis. Additionally, the link to ATP7A trafficking positions these cells to explore copper metabolism’s role in liver cancer progression.
These polyclonal knockout cells support applications such as investigating endosomal recycling and sorting in metastasis, integrin trafficking, and copper homeostasis in HCC. Experimental approaches include western blotting, immunofluorescence, transwell migration, flow cytometry, endocytosis/recycling assays, and co-immunoprecipitation. This model is a valuable resource for mechanistic studies and target validation. For additional product details, usage recommendations, and technical support, please contact Ascent Research.
