The HDAC1 Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited human cell population with targeted disruption of the HDAC1 gene in the TE1 esophageal squamous cell carcinoma (ESCC) line. This polyclonal knockout pool provides a genetically heterogeneous cellular model for investigating histone deacetylase function in a cancer-relevant epithelial setting.
TE1 cells originate from a highly differentiated human ESCC and serve as a widely used model for studying esophageal cancer biology. These adherent epithelial cells exhibit characteristics of malignancy including uncontrolled proliferation and resistance to apoptosis, making them a suitable host for loss-of-function studies.
HDAC1 is a class I histone deacetylase that removes acetyl groups from histone tails and non-histone proteins, thereby regulating chromatin structure and gene expression. In ESCC, HDAC1 is activated by upstream factors such as MYC, E2F1, and NF-??B, and functions within repressor complexes containing SIN3A, NCOR1, MTA1, and HDAC2. It deacetylates substrates like RB1, E2F1, and YY1, and transcriptionally represses tumor suppressors CDKN1A (p21) and pro-apoptotic genes BCL2L11 (Bim) and BAX. Consequently, HDAC1 disruption leads to histone hyperacetylation, derepression of these targets, and induction of cell cycle arrest and apoptosis via p53-dependent and -independent mechanisms. The knockout also impacts signaling through Notch and TGF-?? pathways, which are critical in ESCC progression.
In TE1 polyclonal knockout cells, loss of HDAC1 recapitulates epigenetic reprogramming events that reverse oncogenic gene silencing. This model is valuable for dissecting the role of HDAC1 in sustaining ESCC malignancy, including its interplay with E2F1, p53, and RB1 in cell cycle control and apoptosis. The highly differentiated squamous carcinoma background offers a physiologically relevant platform for testing HDAC inhibitor responses and for exploring the reactivation of silenced tumor suppressive programs.
Typical applications include screening of HDAC inhibitors by assessing histone acetylation marks (H3K9ac, H3K27ac) via Western blot and ChIP-qPCR, transcriptional profiling by RNA-seq and RT-qPCR for CDKN1A, BCL2L11, and TP53, and functional assays such as MTT proliferation, Annexin V apoptosis, colony formation, and migration/invasion studies. The cells are also suited for in vivo xenograft tumor growth evaluation. For assistance, contact Ascent Research.
