EHMT2 Knockout 143B Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population generated from the 143B human osteosarcoma cell line, wherein the EHMT2 gene has been disrupted to eliminate functional protein expression. This loss-of-function model provides a powerful tool for dissecting the epigenetic regulatory roles of EHMT2 in cancer biology without the confounding effects of clonal selection.
The 143B cell line is a well-characterized model of human osteosarcoma, derived from a primary tumor and noted for its highly metastatic and tumorigenic properties. These cells exhibit aggressive growth behavior and are widely employed in studies of bone cancer progression, metastasis, and therapeutic response, making them an ideal host for interrogating the tumor-promoting functions of epigenetic modifiers like EHMT2.
EHMT2 (also known as G9a) catalyzes the mono- and dimethylation of histone H3 at lysine 9 (H3K9me1/me2), a hallmark of facultative heterochromatin and transcriptional repression. It forms stable complexes with EHMT1 and recruits HP1 proteins to establish repressive chromatin domains. Its activity is regulated by upstream signals including MYC, E2F1, TP53, and HIF1A, and it silences key tumor suppressors such as CDKN1A, CDH1, PTEN, and TP53 through direct promoter methylation. EHMT2 also interacts with DNMT1, UHRF1, and ATF7IP to reinforce DNA methylation and stable gene silencing. Through these interactions, EHMT2 integrates multiple oncogenic pathways including Wnt/??-catenin, TGF-??/SMAD, and hypoxia responses, positioning it as a critical node in cancer cell survival.
In the 143B osteosarcoma context, EHMT2-mediated epigenetic silencing contributes to unchecked proliferation, evasion of apoptosis, and enhanced metastatic capacity. Knockout of EHMT2 disrupts H3K9me1/me2 deposition on tumor suppressor loci, potentially restoring expression of CDKN1A and CDH1, thereby attenuating malignant phenotypes. This model thus enables precise dissection of EHMT2??s role in promoting osteosarcoma aggressiveness and in mediating resistance to conventional chemotherapies, as well as its interplay with hypoxia-driven signaling through HIF1A.
Typical applications include chromatin immunoprecipitation (ChIP)-qPCR to profile H3K9me1/me2 enrichment, RT-qPCR and Western blotting to quantify target gene reactivation, and functional assays measuring cell proliferation, migration, and apoptosis. The polyclonal mass population is well suited for drug screening studies with EHMT2 inhibitors such as BIX-01294 and for transcriptomic analyses via RNA-seq to uncover novel downstream targets. This product is intended for research use in academic and pharmaceutical laboratories. For additional details or ordering information, please contact Ascent Research.
