The IKZF5 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population disrupting the IKZF5 gene in human SK-HEP-1 cells. This heterogeneous pool of gene-edited cells provides a loss-of-function model for studying IKZF5-dependent transcriptional regulation without clonal biases. The polyclonal format captures a range of genetic alterations, enabling robust analysis of IKZF5 function in signal transduction and gene expression networks.
The SK-HEP-1 parental line is a human hepatic adenocarcinoma cell line derived from the ascites of a liver adenocarcinoma patient. It exhibits adherent epithelial morphology and co-expresses endothelial and hepatocyte markers, serving as an in vitro model for liver cancer. Its unique phenotype supports investigation of tumor cell plasticity and liver tumor biology, making it a relevant system for studying oncogenic transcription factors.
IKZF5 encodes a zinc-finger transcriptional repressor that recruits chromatin-remodeling complexes through interactions with co-repressors CtBP and HDAC1. It belongs to the IKAROS family and interacts with IKZF1, IKZF3, and IKZF4. IKZF5 operates downstream of the Notch1 intracellular domain (NICD) and IL-7 receptor, and is regulated by transcription factors E2A and EBF1. It represses targets including the cell cycle inhibitor CDKN1A, anti-apoptotic BCL2L1, and the oncogene MYC, thus modulating apoptosis and proliferation. In signaling networks, IKZF5 interfaces with NF-??B components (NFKB1, RELA) and the PI3K/AKT axis (AKT1), linking it to survival pathways.
In SK-HEP-1 cells, IKZF5 knockout likely derepresses tumor suppressor genes and pro-apoptotic factors, potentially shifting the balance toward growth inhibition and cell death. This model enables examination of IKZF5’s role in hepatic transcriptional programs and cross-talk with endothelial-associated pathways. The polyclonal population facilitates detection of phenotype-genotype correlations across diverse mutations, minimizing clonal artifacts and strengthening biological conclusions.
Typical applications include transcriptome profiling via RNA-seq and RT-qPCR to identify IKZF5 target genes, and ChIP-qPCR to validate occupancy at genomic loci. Protein interaction studies using co-immunoprecipitation can probe complexes with CtBP/HDAC1. Functional assays??flow cytometry for apoptosis and cell cycle, MTT proliferation, and Transwell migration/invasion??quantify phenotypic effects. Drug response profiling may reveal altered sensitivity to chemotherapeutics. For further information, please contact Ascent Research.
