The HDAC6 Knockout Ca Ski Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population targeting the HDAC6 gene in the human cervical carcinoma cell line Ca Ski. This polyclonal gene disruption pool provides a heterogeneous cell population with HDAC6 loss-of-function, eliminating the need for single-cell cloning, and serves as a versatile resource for investigating HDAC6-dependent cellular processes.
The parental Ca Ski cell line is an epithelial model derived from a metastasis of a cervical epidermoid carcinoma to the small intestine mesentery. Widely used in cervical cancer research, these cells are particularly suited for studies of tumor invasion, metastasis, and drug resistance, offering a relevant background for dissecting HDAC6 function in oncogenic signaling.
HDAC6 is a cytoplasmic deacetylase that modulates key substrates, including ??-tubulin, cortactin, Hsp90, and peroxiredoxin. Through deacetylation, it regulates microtubule stability, cell motility, and stress responses. Upstream regulators such as p53, Aurora A kinase, and oxidative stress control HDAC6 activity, while interactions with ubiquitin, dynein, p62/SQSTM1, and VCP/p97 link it to aggresome formation and autophagic clearance of ubiquitinated proteins. HDAC6 disruption results in hyperacetylation of its targets, compromising microtubule dynamics, impairing EGFR and TGF-?? signaling-related migration, and disrupting protein quality control pathways.
In Ca Ski cells, HDAC6 knockout removes cytoplasmic deacetylation, causing hyperacetylation of ??-tubulin and cortactin and altering microtubule dynamics. This impairs aggresome processing and autophagic degradation of misfolded proteins, while attenuating the migration and invasion phenotype characteristic of metastatic cervical carcinoma. Thus, this knockout model is a powerful system for linking protein quality control to cancer cell motility.
This knockout product is ideally suited for a wide range of experimental workflows. Representative assays include western blotting to monitor acetylated ??-tubulin levels, transwell migration and invasion assays, immunofluorescence staining for microtubule organization and aggresome accumulation, autophagy flux measurements using LC3-based reporters, co-immunoprecipitation of HDAC6 interactors, and pharmacological profiling with HDAC6-selective inhibitors. The polyclonal nature of the cells enables robust population-level analyses without clonal bias, facilitating drug resistance studies and pooled genetic screens. For detailed protocols or to inquire about this product, please contact Ascent Research.
