The HDAC4 Knockout CAL-27 Polyclonal Cells are a CRISPR/Cas9-mediated gene-disrupted cell population derived from the CAL-27 human tongue squamous cell carcinoma line (Homo sapiens). This polyclonal knockout model provides a functional loss of histone deacetylase 4 (HDAC4), enabling targeted investigation of HDAC4-dependent processes in an oral cancer context.
The CAL-27 parental cell line is an adherent epithelial line established from a human tongue squamous cell carcinoma. These HPV-negative cells serve as a well-established in vitro system for studying molecular mechanisms of oral squamous cell carcinoma, including tumor cell proliferation, migration, invasion, and response to therapeutic agents.
HDAC4 is a class IIa histone deacetylase that represses transcription by deacetylating lysine residues on histone tails (H3, H4) and non-histone substrates such as MEF2 transcription factors and p53. Its subcellular localization and activity are dynamically regulated by phosphorylation: upstream kinases including CaMKII and PKD phosphorylate HDAC4, promoting binding to 14-3-3 chaperones and nuclear export. In the nucleus, HDAC4 assembles into complexes with HDAC3 and the N-CoR/SMRT corepressor to modulate chromatin structure and repress target genes. Key downstream effectors include MEF2-driven gene programs, p53-mediated apoptosis, RUNX2, and HIF-1??, linking HDAC4 to control of cell cycle progression, apoptosis, and differentiation.
In the CAL-27 background, knockout of HDAC4 is anticipated to disrupt these regulatory networks, potentially altering proliferation, survival, and invasive properties of oral squamous cell carcinoma cells. Given HDAC4??s deacetylation of p53 and modulation of MEF2 transcriptional activity, loss of HDAC4 may sensitize cells to apoptotic stimuli or modify their metastatic capacity, making this model useful for dissecting oncogenic signaling and evaluating HDAC inhibitor sensitivity in a disease-relevant context.
These polyclonal knockout cells are suitable for a wide range of applications, including validation of HDAC4 depletion via western blotting and RT-qPCR, transcriptome profiling by RNA-seq, and chromatin immunoprecipitation (ChIP-qPCR) to assess histone acetylation changes. Functional assays can address proliferation (MTT, colony formation), apoptosis (Annexin V), and migration/invasion (Transwell). The model also supports drug sensitivity studies with HDAC inhibitors and immunofluorescence-based analysis of downstream factors like MEF2 localization. For additional information, please contact Ascent Research.
