The HDAC8 Knockout KYSE-150 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population generated from the KYSE-150 human esophageal squamous cell carcinoma line. This product features targeted disruption of the HDAC8 gene, establishing a loss-of-function model without single-cell cloning. The polyclonal format retains inherent cellular heterogeneity, making it ideal for pooled functional genomics and drug screening applications.
KYSE-150 was originally derived from a human esophageal squamous cell carcinoma and is a well-characterized model for studying esophageal cancer biology. These adherent epithelial cells retain hallmark properties of malignancy, including sustained proliferation, migratory potential, and resistance to apoptosis, offering a physiologically relevant system for investigating oncogenic mechanisms and therapy response. The cell line has been employed in numerous studies to elucidate signaling aberrations in esophageal squamous cell carcinoma.
HDAC8 is a class I histone deacetylase that deacetylates histone H3, histone H4, and non-histone substrates such as SMC3, p53, and cortactin. Through these activities, HDAC8 modulates chromatin structure, transcription, sister chromatid cohesion, and cell motility. Its function is regulated by HSP70 and PKA-dependent phosphorylation and involves interactions with the cohesin complex (SMC1A, SMC3, RAD21) as well as NCOR1 and MTA1. Loss of HDAC8 disrupts cohesin dynamics and gene expression, leading to cell cycle arrest and apoptosis.
In this knockout model, removal of HDAC8 activity leads to hyperacetylation of histone H3, H4, and non-histone proteins like SMC3 and p53, thereby destabilizing chromatin architecture and altering gene expression profiles. This disruption is anticipated to hinder cell cycle progression at the G2/M checkpoint, activate apoptotic cascades, and attenuate cell migration??features that are often dysregulated in HDAC8-overexpressing tumors. By reverting these oncogenic phenotypes, the model offers a powerful system for dissecting HDAC8??s contributions to esophageal cancer and for testing synthetic lethal interactions.
This cell population supports diverse experimental applications. Acetyl-histone western blots and acetyl-SMC3 detection confirm HDAC8 disruption, while RT-qPCR profiles downstream gene expression changes. Functional assays such as proliferation, apoptosis, and migration/invasion tests delineate phenotypic consequences, and flow cytometry monitors cell cycle distribution. RNA-seq and immunofluorescence further resolve epigenetic and cohesin localization effects. The model is valuable for HDAC8 inhibitor validation and mechanistic studies. For inquiries, please contact Ascent Research.
