The KDM6A Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human HeLa cervical adenocarcinoma line. This product features targeted disruption of the KDM6A gene, which encodes a histone lysine demethylase. The polyclonal format provides a heterogeneous pool of edited alleles, offering a robust loss-of-function model without clonal bias. Cells are supplied as a live population ready for expansion and experimental use.
HeLa cells are an immortalized epithelial line from a cervical adenocarcinoma, expressing HPV18 oncoproteins E6 and E7, which inactivate p53 and Rb, respectively. This background compromises cell cycle checkpoints and DNA damage responses, making HeLa cells a standard model for studying viral oncogenesis and epigenetic dysregulation. Their widespread use and genetic tractability facilitate investigations into chromatin biology and cancer signaling.
KDM6A demethylates histone H3 at lysine 27, removing repressive H3K27me2/me3 marks to enable transcriptional activation. It functions in complexes with MLL3 (KMT2C) and MLL4 (KMT2D), and interacts with BRG1 (SMARCA4), p53, and beta-catenin. Upstream signals including NOTCH, TGF-beta, and retinoic acid regulate KDM6A activity. Downstream, KDM6A promotes expression of targets such as HOX gene clusters, CDKN2A (p16INK4a), RB1, and E-cadherin, while suppressing N-cadherin and PUMA. Knockout leads to increased H3K27me3 at these loci, disrupting cell cycle, apoptosis, and differentiation.
In the HeLa context, with p53 and Rb already inactivated, KDM6A loss further silences tumor suppressors like CDKN2A and p53 targets, and alters epithelial-mesenchymal transition markers. This model is relevant to cervical cancer, bladder cancer, breast cancer, leukemia, and Kabuki syndrome 2. It enables dissection of epigenetic mechanisms driving malignancy and developmental defects.
Applications include ChIP-qPCR to assess H3K27me3 enrichment, RT-qPCR and RNA-seq for transcriptomic analysis, Western blot for histone modifications, and flow cytometry for cell cycle and apoptosis. Functional assays such as migration/invasion can be performed. The model supports drug target validation and epigenetic compound screening. For further information, contact Ascent Research.
