HDAC6 Knockout LoVo Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population with disrupted HDAC6. This loss-of-function model allows investigation of HDAC6-dependent processes in a genetically defined background. The polyclonal nature provides a heterogeneous pool suitable for pooled functional studies and drug sensitivity profiling, without clonal selection. This product serves as an experimental system for dissecting the roles of this cytoplasmic deacetylase.
The LoVo parental line is a human colon adenocarcinoma cell line derived from a metastatic lymph node. It harbors APC and KRAS mutations with wild-type TP53, driving constitutive Wnt/??-catenin and MAPK signaling. LoVo cells maintain epithelial morphology and are widely used as a colon carcinoma model for invasion, metastasis, and drug response studies. This background makes the line particularly relevant for studying HDAC6 in tumor progression.
HDAC6 encodes a cytoplasmic deacetylase with selectivity for non-histone substrates, including ??-tubulin, cortactin, and HSP90. Deacetylation of ??-tubulin promotes microtubule stability and cell motility, while HSP90 deacetylation modulates client protein stability. It interacts with p62/SQSTM1 and ubiquitin to facilitate aggresome formation and autophagic clearance. Upstream regulators include EGFR, Aurora A kinase, and TGF-??. HDAC6 also deacetylates ??-catenin, providing a link to Wnt signaling. Thus, HDAC6 integrates diverse signals to coordinate cytoskeletal dynamics, proteostasis, and cell survival.
Knockout of HDAC6 in LoVo cells disrupts these critical functions. Loss of ??-tubulin deacetylation impairs cell migration and invasion, which is particularly relevant for metastatic colon carcinoma. Disrupted HSP90 deacetylation destabilizes oncogenic client proteins, attenuating proliferation and survival signaling. The APC/KRAS-mutant background of LoVo cells, combined with HDAC6 loss, may uncover therapeutic vulnerabilities. This model therefore provides a powerful tool for dissecting HDAC6-dependent processes in colon cancer biology.
This polyclonal knockout pool is suited for advanced applications. It enables metastasis studies via migration and invasion assays, and HDAC inhibitor drug screening. Autophagy research benefits from perturbed p62-mediated clearance, while protein quality control studies monitor HSP90 clients. Assays commonly employed include Western blotting and immunofluorescence for acetylated ??-tubulin, co-immunoprecipitation of HSP90 client complexes, flow cytometry for apoptosis, and RNA-seq transcriptomics. For further information, please contact Ascent Research.
