The HDAC4 Knockout Ca Ski Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the HDAC4 gene in the Ca Ski human cervical squamous cell carcinoma line. This loss-of-function model provides a stable genetic background for examining HDAC4-dependent processes without reliance on transient knockdown methods.
Ca Ski is an adherent epithelial cell line derived from a cervical squamous cell carcinoma, carrying integrated HPV-16 genomes. It serves as a key model for HPV-driven oncogenesis, exhibiting features such as deregulated proliferation and apoptosis resistance that are highly relevant to the study of epigenetic regulators in cervical cancer pathogenesis.
HDAC4 is a Class IIa histone deacetylase that represses transcription by deacetylating histones and non-histone proteins including MEF2 transcription factors. Its nucleocytoplasmic shuttling is governed by phosphorylation-dependent binding to 14-3-3 proteins, triggered by upstream kinases CaMKII, CaMKIV, PKA, ERK1/2, and GSK3??. Within the nucleus, HDAC4 associates with corepressors SMRT, NCoR, and HDAC3 to silence targets such as p53, STAT3, HIF-1??, c-fos, Nur77, Bcl-2, and cyclin D1. Consequently, HDAC4 integrates signals from CaMK, MAPK/ERK, TGF-??/SMAD, Wnt/??-catenin, and p53 pathways to modulate cell growth, survival, and differentiation.
In cervical cancer, HDAC4 dysregulation is linked to tumor progression, EMT, and metastasis. This knockout model enables dissection of HDAC4??s role in HPV-16 E6/E7-mediated transformation, including impacts on p53 function and TGF-??/Wnt pathway cross-talk. It also facilitates analysis of HDAC4-dependent chromatin remodeling and transcriptional programs that contribute to therapeutic resistance.
The polyclonal knockout cells are suitable for a range of experimental techniques, including western blotting, RT-qPCR, and HDAC activity assays for validation; cell viability and Annexin V/PI apoptosis assays for phenotypic characterization; migration/invasion assays for EMT studies; immunofluorescence and ChIP-qPCR for spatial and chromatin analysis; RNA-seq for transcriptome-wide profiling; flow cytometry for cell cycle and death analysis; and colony formation or drug sensitivity assays to evaluate clonogenicity and chemoresponse. For technical inquiries, please contact Ascent Research.
