The HDAC8 Knockout SK-HEP-1 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt HDAC8 expression in the human SK-HEP-1 cell line. This knockout pool consists of cells harboring diverse indel mutations introduced by the CRISPR/Cas9 nuclease, collectively resulting in a functional loss of the target protein without the need for clonal selection. The product provides a ready-to-use model for investigating HDAC8-dependent processes in a hepatocellular carcinoma background.
The SK-HEP-1 host cells were originally isolated from the ascitic fluid of a 52-year-old Caucasian male with liver adenocarcinoma. This adherent, epithelial-like cell line is extensively utilized as an in vitro model for hepatocellular carcinoma, retaining relevant genetic and phenotypic features of liver tumorigenesis. Its robust growth characteristics and well-characterized signaling networks make it amenable to a wide array of molecular and cellular assays.
HDAC8 functions as a class I histone deacetylase that removes acetyl groups from lysine residues on histones H3/H4 and critical non-histone proteins, notably SMC3 and p53. Deacetylation of SMC3 by HDAC8 modulates cohesin complex dynamics, essential for mitotic chromosome cohesion, while p53 deacetylation impacts its transcriptional regulation of p21 (CDKN1A). HDAC8 activity is regulated by PKA-mediated phosphorylation at Ser39 and transcriptional control by STAT3, and it requires zinc as a cofactor. This enzyme integrates signals from pathways including Wnt/??-catenin, TGF-??/SMAD, and STAT3, positioning it as a central node linking epigenetic modifications to cell proliferation, apoptosis, and genomic stability.
In hepatocellular carcinoma, HDAC8 dysregulation contributes to oncogenic transformation and disease progression. The SK-HEP-1 knockout model enables researchers to dissect the consequences of HDAC8 loss in a hepatic adenocarcinoma context, where impaired deacetylation of SMC3 and p53 is anticipated to disrupt cohesin function and activate p53-mediated growth suppression. This system thus facilitates the investigation of HDAC8-driven mechanisms in liver cancer cell survival, migration, and therapeutic resistance.
This polyclonal knockout cell population is suited for functional genomics, epigenetic research, and drug discovery applications. Users can validate target disruption via Western blotting, RT-qPCR, and Sanger sequencing. Acetylation status of SMC3 and p53 can be examined by immunofluorescence or acetylation-specific assays. Effects on proliferation, apoptosis, and cell cycle can be assessed through MTT assay, Annexin V staining, and flow cytometry. Additionally, ChIP-qPCR can reveal histone acetylation changes at gene promoters. These tools support HDAC8 inhibitor screening and mechanistic studies of cohesin biology in cancer. For more information, contact Ascent Research.
