The HDAC8 Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the TE1 human esophageal squamous cell carcinoma line, engineered to harbor a targeted disruption of the histone deacetylase 8 (HDAC8) gene. This product is supplied as a mixed population of cells with heterogeneous HDAC8 knockout alleles, generated by transient delivery of CRISPR/Cas9 components, and serves as a loss-of-function model for studying HDAC8-mediated epigenetic regulation and tumor cell biology.
The TE1 cell line originates from a human esophageal squamous cell carcinoma and is widely employed as a model system for investigating esophageal cancer pathogenesis, drug response, and molecular mechanisms. These cells exhibit characteristic features of squamous cell carcinoma, including aggressive growth and altered signaling networks, making them particularly suitable for functional interrogation of genes implicated in esophageal tumorigenesis.
The HDAC8 protein functions as a class I histone deacetylase that catalyzes the removal of acetyl groups from lysine residues on core histones H3 and H4, as well as non-histone substrates such as the tumor suppressor p53 and the cohesin complex component SMC3. Through its deacetylase activity, HDAC8 promotes chromatin condensation and transcriptional repression, while also modulating protein stability and interactions. Upstream regulators including p53, hypoxia-inducible factors, and microRNAs such as miR-21 and miR-200b control HDAC8 expression levels. HDAC8 interacts with the cohesin complex, nuclear receptor corepressors, HSP70, and STAT3, facilitating dynamic regulation of cell cycle progression, apoptosis, and cell adhesion. Downstream deacetylation events affect p53 transcriptional activity, SMC3-mediated sister chromatid cohesion, and the expression of cell cycle regulators p21 and Bcl-2.
Disruption of HDAC8 in TE1 cells is anticipated to perturb histone acetylation homeostasis and transcriptional programs governing proliferation and survival. Consistent with its mechanistic role, HDAC8 knockout is predicted to induce p53 hyperacetylation, thereby enhancing its transcriptional activity and leading to upregulation of p21, a cyclin-dependent kinase inhibitor that arrests cell cycle progression. This may also lower the threshold for apoptosis, as evidenced by altered Bcl-2 family expression. In the context of esophageal squamous cell carcinoma, such molecular changes render this knockout model valuable for dissecting HDAC8-dependent oncogenic pathways and for evaluating the therapeutic potential of HDAC inhibitors.
This polyclonal knockout cell population is suitable for a range of research applications, including drug screening studies aimed at identifying selective HDAC8 inhibitors, epigenetic profiling, and tumor biology investigations. Researchers can employ western blotting to assess HDAC8 ablation and acetylation status of histones H3/H4 and p53, RT-qPCR to quantify target gene expression changes (e.g., p21, Bcl-2), flow cytometry to monitor cell cycle distribution and apoptosis, and functional assays such as proliferation, migration, and invasion to evaluate tumor cell behavior. Additionally, this model supports HDAC activity measurements and immunofluorescence staining for acetylated histone marks. For further technical details or to discuss customization options, please contact Ascent Research.
