The HDAC6 Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human TE1 esophageal squamous cell carcinoma line, enabling loss-of-function studies of HDAC6, a cytoplasmic deacetylase. This heterogeneous pool harbors targeted disruption of the HDAC6 gene without clonal isolation, providing a model that reflects tumor cell variability. HDAC6 is central to cytoskeletal regulation and protein homeostasis, making this tool relevant for cancer biology investigations.
The TE1 cell line is a well-characterized model of esophageal squamous cell carcinoma, retaining migratory and invasive properties alongside oncogenic signaling networks. Originating from a human esophageal tumor, TE1 cells are extensively used in preclinical research on esophageal cancer pathology and therapeutic responses. The esophageal cancer derivation positions the HDAC6 knockout derivative as a pertinent system for examining HDAC6 contributions to malignant phenotypes, including motility and stress adaptation.
HDAC6 is a cytoplasmic deacetylase that targets ??-tubulin and HSP90, modulating microtubule dynamics, protein stability, and the aggresome-autophagy pathway. Its activity is regulated by EGFR, TGF-??, hypoxia, NF-??B, STAT3, and oxidative stress, leading to changes in ??-tubulin and HSP90 acetylation, cortactin deacetylation, and microtubule stability. HDAC6 interacts with ubiquitin, p62/SQSTM1, the dynein motor complex, cortactin, and tau to coordinate misfolded protein trafficking and autophagic clearance. Thus, HDAC6 integrates growth factor and stress signals to control cell migration and proteotoxic stress responses.
In esophageal squamous cell carcinoma, HDAC6 upregulation promotes cell migration, invasion, and resistance to proteotoxic stress. Knocking out HDAC6 in TE1 cells impairs motility and sensitizes cells to proteotoxic agents. The polyclonal knockout format maintains parental heterogeneity, allowing population-level analyses and minimizing clonal selection artifacts. This model therefore offers a clinically relevant platform for studying HDAC6-dependent mechanisms in esophageal cancer progression.
Key applications include investigating HDAC6??s role in esophageal cancer migration and invasion, probing the aggresome-autophagy pathway, screening HDAC6 inhibitors, analyzing microtubule-dependent processes, and assessing chemosensitivity. Typical assays involve Western blotting for acetylated ??-tubulin and HSP90, wound healing migration assays, immunofluorescence for microtubule bundling, autophagy flux measurements, and MTT viability tests with HDAC6 inhibitors. For further details and ordering, contact Ascent Research.
