The HDAC8 Knockout CAL-27 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population generated by disrupting the HDAC8 gene in the CAL-27 tongue squamous carcinoma line. This heterogeneous pool provides a loss-of-function model free from clonal selection artifacts, supplied as a polyclonal population to preserve genetic diversity for robust functional and biochemical studies.
The parental CAL-27 cell line, derived from a tongue squamous cell carcinoma of a 56-year-old male, is an adherent, HPV-negative epithelial model widely used in oral cancer research. It retains oncogenic pathway activation (NF-??B) and dysregulated cell cycle control, making it a physiologically relevant background for studying HDAC8 tumor-suppressive functions.
HDAC8 functions as a histone deacetylase that deacetylates histone H4K16 and non-histone substrates p53 and SMC3. Its activity is modulated by upstream regulators including p53, c-Myc, NF-??B, and microRNAs (miR-346, miR-145). Deacetylation of SMC3 impacts sister chromatid cohesion, while deacetylation of p53 suppresses transactivation of p21 and Bcl-2. HDAC8 forms complexes with cohesin proteins (SMC3, RAD21, SMC1A) and with p53, ERR??, CREB, and HSP70, linking Notch, p53, and NF-??B signaling. Disruption of HDAC8 leads to hyperacetylation of H4K16, p53, and SMC3, culminating in p53 reactivation, G1 arrest, and intrinsic apoptosis.
In CAL-27 oral squamous carcinoma cells, HDAC8 knockout elevates acetylation of H4K16, p53, and SMC3, promoting chromatin relaxation and p53-driven transcription. This upregulates p21 to enforce G1 arrest and shifts Bcl-2 family balance toward intrinsic apoptosis. With wild-type p53, CAL-27 is ideal for distinguishing p53-dependent and -independent HDAC8 functions. The interplay with Notch and NF-??B in this model further clarifies HDAC8??s role in tumor maintenance and therapy response.
The HDAC8 Knockout CAL-27 Polyclonal Cells are suitable for functional studies including colony formation, wound healing, and Annexin V apoptosis assays. The polyclonal format facilitates high-throughput screening of HDAC8 inhibitors, with readouts such as Western blot for acetyl-H4K16 and acetyl-p53, and RT-qPCR for p21. Additionally, these cells enable ChIP-seq and RNA-seq analyses to map genome-wide acetylation and transcriptome changes. Researchers investigating HDAC8 interactions with p53, NF-??B, or Notch can employ this model to dissect signaling mechanisms and evaluate drug sensitivity in oral cancer. For further details or to request a quote, please contact Ascent Research.
