The EHMT2 Knockout MCF-7 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the MCF-7 human breast adenocarcinoma cell line. This product provides a heterogeneous pool of cells with targeted disruption of the EHMT2 gene, enabling loss-of-function studies without the biases of single-cell clonal selection.
The MCF-7 parental line is an estrogen receptor-positive (ER+), progesterone receptor-positive (PR+) human breast adenocarcinoma epithelial cell line of the luminal A molecular subtype, originally isolated from a pleural effusion of a metastatic breast cancer patient. These hormone-responsive cells are widely employed as a model system for studying endocrine-dependent breast cancer, owing to their faithful recapitulation of signaling networks driven by estrogen signaling and their sensitivity to anti-estrogen therapies.
EHMT2 (also known as G9a) encodes a histone H3K9 methyltransferase that catalyzes H3K9me1/me2, marks associated with transcriptional silencing. In MCF-7 cells, EHMT2 forms repressive complexes with EHMT1, HP1??, CtBP, LSD1, WIZ, and CDYL. It is regulated by upstream factors E2F1, MYC, HIF1??, and AKT, and represses tumor suppressor genes including CDKN1A (p21), CDH1 (E-cadherin), PTEN, DLC1, and RUNX3. EHMT2 integrates signals from Wnt/??-catenin, TGF-??, NF-??B, and p53 pathways; its activity modifies chromatin at promoters where ??-catenin/TCF/LEF, SMAD2/3, p65, and p53 complexes control gene expression. CRISPR/Cas9-mediated disruption of EHMT2 therefore removes H3K9me1/2, relieving repression of these suppressors and reversing oncogenic programs.
In the MCF-7 breast cancer model, EHMT2-mediated epigenetic silencing contributes to the malignant phenotype by suppressing genes that restrain cell proliferation, migration, and survival. Loss of EHMT2 function in this polyclonal knockout population is expected to re-express silenced tumor suppressors, such as E-cadherin and p21, thereby impairing cell cycle progression and enhancing cell adhesion. This model provides a powerful tool for dissecting how epigenetic dysregulation drives estrogen receptor-positive breast cancer and for evaluating the therapeutic potential of targeting G9a in hormone-responsive tumors.
This polyclonal knockout cell product is ideally suited for a broad range of epigenetic and cancer biology investigations. Researchers can employ western blotting to confirm reduction in H3K9me1/2 marks and upregulation of target proteins such as CDH1 or CDKN1A. RT-qPCR enables quantitative analysis of de-repressed transcript levels, while ChIP-qPCR can be used to map changes in H3K9me2 occupancy at specific gene promoters. Functional assays, including MTT-based proliferation measurements and transwell migration assays, allow assessment of phenotypic consequences of EHMT2 loss. Moreover, RNA-seq and other genome-wide approaches can be applied to profile global transcriptomic and epigenomic alterations. These cells are a valuable resource for drug target discovery, validation of epigenetic therapies, and mechanistic studies of chromatin regulation in breast cancer. For additional information or custom inquiries, please contact Ascent Research.
