The HDAC6 Knockout HT29 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human HT29 colorectal adenocarcinoma cell line, designed to disrupt HDAC6 gene function. This pooled format provides a robust loss-of-function model for investigating the cytoplasmic deacetylase HDAC6, facilitating studies into its roles in microtubule dynamics, protein degradation, and cell motility without the selection bias of clonal isolates.
HT29 cells originate from a 44-year-old female with colorectal adenocarcinoma and are widely employed as an intestinal epithelial model in cancer research, drug screening, and barrier function assays. Their well-characterized signaling networks and epithelial phenotype make them highly tractable for genetic manipulation and subsequent phenotypic analysis in colorectal cancer and related pathologies.
HDAC6 is a unique cytoplasmic deacetylase that primarily targets non-histone substrates, including ??-tubulin, HSP90, and cortactin, thereby regulating microtubule stability, protein chaperoning, and actin cytoskeleton remodeling. Key upstream regulators such as EGF, EGFR, AKT, ERK, and IL-6 modulate HDAC6 activity, while downstream consequences include altered acetylation of ??-tubulin and HSP90, impacting microtubule-dependent transport and protein complex formation. HDAC6 physically interacts with ubiquitin, p62/SQSTM1, dynein motor complex, Tau, and HSP90, and plays a critical role in aggresome formation by linking ubiquitinated cargo to dynein-driven retrograde transport.
In the HT29 cellular context, disruption of HDAC6 results in hyperacetylation of ??-tubulin, impaired aggresome formation, and aberrant responses to stress and growth factor signaling. These alterations provide a clinically relevant platform for dissecting colorectal cancer progression, as HDAC6 influences EGFR and NF-??B pathways often dysregulated in tumorigenesis, and its knockout can shift autophagy and protein degradation dynamics, offering insights into therapeutic resistance mechanisms.
This polyclonal knockout cell population supports a diverse range of experimental applications, including western blotting for acetylated ??-tubulin, immunofluorescence analysis of microtubule organization, migration and invasion assays, autophagy flux measurements, and sensitivity profiling with HDAC inhibitors. It is ideally suited for research into colorectal cancer biology, aggresome-autophagy crosstalk, and epigenetic drug discovery. For further information or custom inquiries, please contact Ascent Research.
