The DNMT3A Knockout CAL-27 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population engineered from the human tongue squamous cell carcinoma line CAL-27, targeting the DNMT3A gene. Disruption of DNMT3A eliminates de novo DNA methyltransferase activity, leading to genome-wide hypomethylation and the re-expression of methylation-silenced genes. The polyclonal format offers a heterogeneous pool of knockout cells, minimizing clonal artifacts and enabling robust population-level analyses.
CAL-27 is a well-characterized epithelial cell line derived from a human oral squamous cell carcinoma of the tongue. It is extensively used as an in vitro model for oral cancer research, retaining hallmark features such as anchorage-independent growth, invasiveness, and tumorigenicity. Its genetic tractability and relevance to oral carcinogenesis make it an ideal host for investigating epigenetic perturbations.
The DNMT3A protein is a key de novo DNA methyltransferase that establishes methylation patterns during development and in disease. It functions within a multi-subunit complex containing the accessory factor DNMT3L, the ubiquitin-like protein UHRF1, histone deacetylases HDAC1/2, and methyl-CpG-binding protein MBD2. Upstream regulation of DNMT3A involves transcription factors SP1 and SP3, and signaling through MAPK and PI3K/AKT pathways, with cytokine interleukin-6 providing additional modulation. Downstream, DNMT3A-mediated hypermethylation silences tumor suppressor loci including CDKN2A and RASSF1, and its activity is counterbalanced by TET dioxygenases. Through these interactions, DNMT3A influences chromatin remodeling and gene expression programs central to cellular differentiation and oncogenesis.
In oral squamous cell carcinoma, aberrant DNMT3A activity contributes to the epigenetic silencing of critical tumor suppressors, promoting neoplastic progression. The knockout of DNMT3A in CAL-27 cells provides a relevant platform to dissect the functional consequences of loss of de novo methylation in an oral cancer context. Researchers can investigate how hypomethylation alters cell proliferation, migration, and apoptosis, and how it modulates sensitivity to chemotherapeutic agents, offering mechanistic insights into epigenetic therapy of oral cancer.
This product is applicable to a broad spectrum of epigenetic research, including analysis of DNA methylation dynamics, reactivation of silenced tumor suppressor genes, and screening of epigenetic drugs. Representative experimental workflows include Western blotting for DNMT3A, RT-qPCR of target genes, bisulfite sequencing for methylation profiling, and functional assays such as MTT proliferation, colony formation, transwell migration, and Annexin V apoptosis. For additional information and ordering, please contact Ascent Research.
