The HERC2 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with disruption of the HERC2 gene in the SK-HEP-1 human hepatic adenocarcinoma cell line. This heterogeneous pool of gene-edited cells provides a loss-of-function model for studying HERC2-dependent processes, avoiding the need for clonal isolation. The polyclonal format maintains genetic diversity while achieving functional ablation of HERC2, suitable for population-based assays in DNA damage response and cancer research.
SK-HEP-1 is a hepatic adenocarcinoma cell line established from the ascitic fluid of a patient with liver adenocarcinoma. Although historically misidentified as endothelial, molecular profiling has confirmed its hepatic origin, and it displays epithelial morphology and tumorigenicity. As a widely used hepatocellular carcinoma model, SK-HEP-1 enables investigations into liver cancer biology, drug sensitivity, and metastasis, providing a disease-relevant background for HERC2 knockout studies.
HERC2 encodes an E3 ubiquitin ligase critical for DNA damage repair and protein degradation. Upon DNA breaks, ATM kinase phosphorylates HERC2, promoting its association with the BRCA1/BARD1 complex to facilitate homologous recombination. HERC2 also ubiquitinates RNF168, modulating histone ubiquitination and recruitment of 53BP1 and BRCA1 to damage sites. The ligase is negatively regulated by NEURL4 and stabilized by USP20, and it influences p53-mediated apoptosis and centrosome function. This signaling network underscores HERC2??s pivotal role in maintaining genomic stability.
In hepatic adenocarcinoma, HERC2 likely acts as a tumor suppressor by safeguarding DNA repair fidelity. Its knockout in SK-HEP-1 cells impairs the DNA damage response, leading to elevated genomic instability??a key driver of liver cancer progression. This model permits dissection of HERC2??s involvement in cell cycle checkpoint control, apoptotic signaling, and responsiveness to genotoxic stress. By eliminating HERC2 in a liver tumor context, researchers can identify synthetic lethal interactions and explore therapeutic vulnerabilities specific to hepatocellular carcinoma.
The polyclonal HERC2 knockout cells are suited for diverse applications, including analysis of DNA repair by ??H2AX/53BP1 immunofluorescence and comet assays, investigation of ubiquitin-dependent signaling via co-immunoprecipitation and Western blotting, and drug sensitivity screening using cell viability and colony formation assays. Additional assays such as flow cytometric cell cycle analysis, Annexin V apoptosis detection, and RNA-seq transcriptomics can delineate downstream consequences of HERC2 loss. This product also supports research into HERC2-related pigmentation and neurological disorders. For further details, please contact Ascent Research.
