The EED Knockout HGC-27 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout cell population targeting the EED gene within the HGC-27 human gastric carcinoma line. This heterogeneous loss-of-function model is generated via CRISPR/Cas9-mediated gene disruption, providing a robust tool for investigating EED-dependent pathways without clonal selection bias.
HGC-27 is an epithelial cell line established from a lymph node metastasis of a poorly differentiated gastric adenocarcinoma. It is widely employed as a model for gastric cancer research, particularly suited for studying genes involved in tumor progression and epigenetic deregulation due to its metastatic origin and aggressive phenotype.
EED functions as a core component of the Polycomb Repressive Complex 2 (PRC2), where it binds trimethylated lysine 27 on histone H3 (H3K27me3) and allosterically activates the methyltransferase EZH2, thereby propagating H3K27me3 marks and enforcing gene silencing. EED interacts with PRC2 subunits SUZ12, RBBP4, and RBBP7, and its activity is modulated by upstream regulators including JARID2, AEBP2, the non-coding RNA HOTAIR, Xist, and pre-existing H3K27me3. Downstream, EED-dependent PRC2 activity leads to deposition of H3K27me3 across the genome, resulting in transcriptional repression of target genes such as the tumor suppressors CDKN2A and CDKN2B. Consequently, EED knockout disrupts this silencing machinery, preventing the feed-forward maintenance of H3K27me3.
In the HGC-27 gastric cancer line, EED loss relieves PRC2-mediated repression of tumor suppressors, providing a disease-relevant model to study how epigenetic silencing contributes to gastric carcinoma pathogenesis. The polyclonal knockout design avoids clonal artifacts and is particularly advantageous for studies requiring population-averaged responses, such as drug sensitivity assays or bulk omics profiling.
This polyclonal knockout cell population enables a wide range of assays: ChIP-qPCR to quantify H3K27me3 changes, RT-qPCR for target gene expression, Western blotting for EED and complex components, colony formation to assess proliferation, and RNA-seq for transcriptome-wide effects. It is also suitable for PRC2 inhibitor dose-response studies and co-immunoprecipitation to evaluate PRC2 integrity. For further assistance, please contact Ascent Research.
