The EHMT2 Knockout KYSE-150 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the EHMT2 gene, providing a loss-of-function model for epigenetic studies in esophageal squamous cell carcinoma. This polyclonal format eliminates the need for single-cell cloning and captures a spectrum of genetic edits, enabling robust functional analyses.
The KYSE-150 cell line, derived from a human esophageal squamous cell carcinoma, is a widely used model for investigating ESCC biology. These adherent epithelial cells exhibit characteristics of squamous cell carcinoma, making them suitable for dissecting oncogenic signaling, proliferation, and therapeutic vulnerabilities.
EHMT2 (G9a) is a histone-lysine N-methyltransferase that methylates histone H3 at lysine 9 to generate H3K9me1/me2/me3, marks recognized by HP1 and associated with transcriptional repression. It functions in complexes with EHMT1, DNMTs, MBD2, and PRC2 components, integrating DNA and histone methylation. Upstream regulators include MYC, E2F1, and PI3K/AKT pathways. EHMT2 deposits H3K9me2 at promoters of tumor suppressors like CDKN1A and CDH1, silencing their expression and promoting proliferation. It also contributes to WNT signaling, DNA repair, and cellular senescence.
In ESCC, EHMT2 is often overexpressed, driving tumor progression through epigenetic silencing. The KYSE-150 background provides a disease-relevant context in which knockout of EHMT2 can reactivate tumor suppressor programs, revealing mechanisms of epigenetic dysregulation. This model is valuable for examining the role of EHMT2 in proliferation, apoptosis, and drug response.
Applications include western blot for H3K9me2/me3, ChIP-qPCR at specific loci, RT-qPCR for CDKN1A and CDH1, RNA-seq, and functional assays such as proliferation, colony formation, and apoptosis. These cells are also useful for testing EHMT2 inhibitors like UNC0642 and BIX-01294, and for target validation studies in cancer epigenetics. For more information, contact Ascent Research.
