The IFRD1 Knockout SK-HEP-1 Polyclonal Cells represent a pool of SK-HEP-1 hepatocellular carcinoma cells that have been subjected to CRISPR/Cas9-mediated genome editing to disrupt the human IFRD1 gene. This polyclonal knockout population offers a heterogeneous genetic background with targeted loss-of-function of the IFRD1-encoded transcriptional corepressor. The product is intended for loss-of-function studies, enabling researchers to interrogate the biological consequences of IFRD1 deficiency without clonal selection artifacts. As a mixed population, it retains the phenotypic diversity of the host line while providing robust gene disruption across the culture.
The SK-HEP-1 host cell line was originally established from the ascites of a patient with liver adenocarcinoma. It displays a unique mixed epithelial and endothelial phenotype, making it a valuable model for hepatocellular carcinoma research. SK-HEP-1 cells exhibit both adherent and non-adherent growth characteristics and express markers of both lineages, facilitating investigations into tumor heterogeneity, metastasis, and endothelial-mesenchymal transition. The cell line is widely adopted for hepatic cancer drug screening, signaling pathway analysis, and functional gene studies.
IFRD1 (interferon-related developmental regulator 1) functions as a transcriptional corepressor that modulates muscle differentiation, inflammatory responses, and cell cycle progression. It recruits histone deacetylases HDAC1 and HDAC3, along with the co-repressor SIN3A, to gene promoters, leading to chromatin condensation and transcriptional silencing. IFRD1 represses myogenic transcription by inhibiting MYOD1 and MEF2-dependent activity, and suppresses NF-??B signaling via interactions with NFKB1 and RELA. Upstream regulators include interferon gamma, tumor necrosis factor alpha, lipopolysaccharide, and Notch pathway components, converging on downstream targets such as MYOG, CDKN1A, and MEF2C.
In SK-HEP-1 hepatocellular carcinoma cells, loss of IFRD1 may disrupt the balance between oncogenic signals and differentiation programs. The model is relevant for examining hepatocyte proliferation versus differentiation, given IFRD1’s role in cell cycle regulation. Additionally, because IFRD1 modulates NF-??B activity, its knockout could affect inflammatory cytokine responses and apoptosis resistance in liver cancer. This system enables exploration of how the corepressor contributes to hepatic tumorigenesis and potential crosstalk between muscle-related pathways and hepatocellular carcinoma.
Researchers can employ this polyclonal knockout cell pool in a broad range of experimental workflows. Applications include the investigation of muscle differentiation mechanisms through reporter gene assays and differentiation assays, the study of inflammatory gene regulation via RT-qPCR and chromatin immunoprecipitation, and the modeling of cystic fibrosis?Crelevant inflammatory phenotypes. In hepatocellular carcinoma research, the cells are suited for proliferation and migration assays, as well as drug screening studies. Compatible analytical methods encompass Western blotting, co-immunoprecipitation, and immunofluorescence microscopy. For further details or to discuss customization options, please contact Ascent Research.
