The HDAC1 Knockout Ca Ski Polyclonal Cells product consists of a CRISPR/Cas9-edited population of Ca Ski cervical carcinoma cells with targeted disruption of the HDAC1 gene. This loss-of-function model enables investigation of histone deacetylase 1 (HDAC1) functions in an HPV16-positive epithelial background. The polyclonal nature preserves a diverse allelic landscape generated by Cas9-mediated DNA cleavage and non-homologous end joining, allowing gene function studies without clonal selection bias. This knockout cell population is suitable for applications including tumor suppressor derepression studies, epigenetic drug screening, and signaling pathway analysis.
Ca Ski cells were derived from a metastatic cervical epidermoid carcinoma and harbor integrated HPV16 genomes, expressing the viral oncoproteins E6 and E7. They grow as adherent monolayers and display hallmark cervical carcinoma features, including dysregulated cell cycle and apoptosis resistance. The HPV16 positivity provides clinical relevance, as high-risk HPV is a major cause of cervical carcinogenesis. Ca Ski cells are thus widely used for studying host?Cvirus interactions and testing therapies for HPV-associated malignancies.
HDAC1 is a transcriptional corepressor that deacetylates histones H3/H4, promoting chromatin condensation and gene silencing. It is regulated by CK2 and PKA phosphorylation and integrates into Sin3, NuRD (MTA2, Mi-2), and CoREST complexes. These complexes are recruited by E2F1, p53, Sp1, and YY1 to repress targets like p21, p27, and Bim, while also modulating E-cadherin. Thus, HDAC1 connects Notch, Wnt, TGF-beta, and p53 signals, serving as a critical node in cell cycle and developmental control.
In Ca Ski cells, HDAC1 supports the transformed phenotype by silencing pro-apoptotic and antiproliferative genes, a function potentially intensified by HPV oncoproteins. Its disruption enables dissection of epigenetic drivers in cervical cancer and assessment of deacetylase dependency. This model is therefore valuable for studying restoration of tumor suppressors and apoptotic sensitization upon HDAC1 inhibition, facilitating preclinical evaluation of HDAC-targeted therapies.
This knockout polyclonal cell product supports western blotting for HDAC1 and apoptosis markers, RT-qPCR for target gene expression, ChIP-qPCR for histone acetylation, cell proliferation assays, and HDAC inhibitor sensitivity testing. Immunofluorescence can visualize global acetylation changes. These approaches allow thorough epigenetic and functional characterization. Please contact Ascent Research for further information.
