The HDAC1 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the CAL-27 human tongue squamous cell carcinoma line, providing a loss-of-function model for histone deacetylase 1 (HDAC1). This polyclonal pool, generated through CRISPR/Cas9-mediated gene disruption, comprises a heterogeneous mixture of cells lacking functional HDAC1, enabling unbiased investigation of HDAC1-dependent processes without clonal artifacts.
CAL-27 is an epithelial cell line established from a 56-year-old male with tongue squamous cell carcinoma, widely used as an oral cancer model. It retains salient features of the disease, including deregulated proliferation and apoptosis, making it a relevant host for studying the epigenetic contributions of HDAC1 in oral squamous cell carcinoma pathobiology.
HDAC1 encodes a class I histone deacetylase that removes acetyl groups from lysine residues on histone H3 and H4 tails, driving chromatin condensation and transcriptional silencing. It functions within multiprotein repressor complexes such as SIN3A, NuRD, and CoREST, interacting with factors like MTA2, Rb, and MECP2. HDAC1 activity is regulated by upstream signals including E2F transcription factors, MYC, p53, CK2 kinase, and Aurora A kinase. Its deacetylase activity represses tumor suppressor genes such as p21 (CDKN1A) and p53, while modulating the function of E2F1 and STAT3. By integrating inputs from Wnt (beta-catenin), Notch (Notch intracellular domain), p53, and TGF-beta pathways, HDAC1 orchestrates transcriptional programs that control cell cycle progression and apoptosis.
In the CAL-27 oral cancer background, HDAC1-mediated epigenetic silencing promotes malignant behavior by suppressing pro-apoptotic and growth-inhibitory targets. Disruption of HDAC1 in this polyclonal knockout population is predicted to reactivate repressed genes, such as p21, and increase histone acetylation, offering a platform to dissect HDAC1-dependent gene regulation and assess reliance on HDAC1 for tumor cell survival.
Applications include ChIP-qPCR for histone H3 acetylation, RT-qPCR and Western blotting for p21 and other target expression, and functional analyses including proliferation, apoptosis, cell cycle, and colony formation assays. These cells are apt for HDAC inhibitor screening and transcriptional reprogramming studies. For further information, contact Ascent Research.
