The ING2 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ING2 tumor suppressor gene in the human SK-HEP-1 hepatocellular carcinoma cell line. This polyclonal format provides a heterogeneous loss-of-function model that circumvents clonal selection bias, enabling population-based analyses of ING2 ablation in liver cancer contexts and investigation of p53-mediated signaling, cell cycle regulation, and apoptosis.
The SK-HEP-1 line is an established malignant liver adenocarcinoma cell line derived from patient ascites, exhibiting key features of hepatocellular carcinoma including dysregulated proliferation and apoptotic resistance. As a widely used HCC research model, it enables the study of oncogenic pathways and tumor suppressor functions. The introduction of ING2 knockout allows precise dissection of gene-specific contributions to hepatocarcinogenesis and therapeutic response within a clinically relevant background.
ING2 functions as a tumor suppressor by binding trimethylated histone H3 at lysine 4 (H3K4me3) via its PHD domain, localizing to active chromatin where it enhances p53 acetylation. This modification increases p53 transcriptional activity, driving expression of the cyclin-dependent kinase inhibitor p21/CDKN1A and the pro-apoptotic factor BAX, thereby inducing cell cycle arrest and apoptosis. ING2 also interacts with the mSin3a-HDAC corepressor complex through SAP30 and RbBP4, contributing to local histone deacetylation and transcriptional repression. Its activity is regulated upstream by DNA damage response pathways and miR-214.
In hepatocellular carcinoma, the ING2-p53 tumor suppressor axis is frequently disrupted, promoting unchecked growth and survival. The SK-HEP-1 ING2 knockout model provides a physiologically relevant system to elucidate p53-dependent and -independent functions of ING2, explore epigenetic cross-talk, and investigate drug sensitivities that arise from ING2 loss. The polyclonal nature mimics intratumoral heterogeneity, strengthening its translational utility for studying liver cancer pathogenesis and therapeutic liabilities.
This knockout cell population supports diverse assays including western blotting and RT-qPCR for target validation, MTT/CCK-8 proliferation assays, Annexin V apoptosis detection, and cell cycle flow cytometry. p53 transcriptional activity can be measured by luciferase reporter, while protein interactions are probed via co-immunoprecipitation and immunofluorescence. The model is also suited for drug sensitivity profiling and chromatin immunoprecipitation studies of H3K4me3 occupancy. For detailed technical information, contact Ascent Research.
