The EHMT2 Knockout SK-OV-3 Polyclonal Cells product provides a CRISPR/Cas9-mediated polyclonal knockout population derived from the SK-OV-3 human ovarian adenocarcinoma cell line. The pool comprises cells with targeted disruption of the EHMT2 gene, generating a heterogeneous loss-of-function model for epigenetic research. Unlike clonal lines, this polyclonal format retains population-level diversity while uniformly abrogating EHMT2 protein expression, enabling robust functional studies without the bias of single-cell selection.
The SK-OV-3 parental line originates from a human ovarian serous cystadenocarcinoma and exhibits epithelial morphology. This cell line is a well-established model for high-grade serous ovarian cancer, widely used to investigate oncogenic signaling, drug resistance, and metastasis. Its genetic background includes TP53 mutation and aberrations in PI3K/AKT and Wnt/??-catenin pathways, making it particularly suitable for examining the crosstalk between genetic lesions and epigenetic modifiers such as EHMT2.
EHMT2 (G9a) is a histone lysine methyltransferase that catalyzes mono- and dimethylation of histone H3 at lysine 9 (H3K9me1/2), leading to transcriptional repression. It functions within a multimeric complex containing EHMT1 (GLP), WIZ, and corepressors CtBP and HDAC1/2, and recruits HP1 (CBX5) to propagate heterochromatin. EHMT2 is regulated upstream by E2F1, c-Myc, HIF1A, AKT signaling, and miR-217. Its major downstream targets include promoter H3K9me2 at CDH1 (E-cadherin) and CDKN1A (p21), silencing these tumor suppressors. Additionally, EHMT2 methylates p53 at lysine 373 to attenuate its transcriptional activity, and its activity promotes epithelial-mesenchymal transition (EMT), proliferation, and survival. Inhibition or knockout restores expression of silenced genes.
In the SK-OV-3 ovarian cancer context, EHMT2 knockout disrupts this repressive network, leading to reactivation of CDH1 and CDKN1A, thereby inhibiting EMT, cell proliferation, and migration. The polyclonal knockout population allows assessment of these phenotypic changes without clonal artifacts, providing a physiologically relevant system to study epigenetic tumor suppressor reactivation. This model is instrumental for dissecting the role of H3K9 methylation in ovarian cancer progression and for evaluating the therapeutic potential of EHMT2 inhibitors. Moreover, it enables investigation of the interplay between EHMT2 and DNA methyltransferases (DNMT1, DNMT3A) in coordinating gene silencing.
Research applications include chromatin immunoprecipitation (ChIP-qPCR) to map changes in H3K9me2 at target promoters, immunofluorescence to visualize global H3K9me2 levels, and co-immunoprecipitation to probe EHMT2-containing complexes. Functional assays such as proliferation, apoptosis, and migration analyses quantify anti-tumor effects, while RNA-seq and inhibitor sensitivity testing support drug discovery and target validation. This knockout model is also suitable for studying autophagy and TGF-??/p53 signaling pathways in ovarian cancer. Please contact Ascent Research for further information.
