The EED Knockout HCT 116 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population engineered to disrupt the EED gene in the human HCT 116 colorectal carcinoma cell line. This product provides a loss-of-function model to study the essential core component of the Polycomb Repressive Complex 2 (PRC2). The polyclonal format ensures a heterogeneous knockout population, enabling robust functional screening and pooled analyses without clonal selection bias.
HCT 116 cells are derived from a human colorectal adenocarcinoma and exhibit microsatellite instability (MSI?H) along with a KRAS G13D mutation and wild?type TP53 status. This genetic background makes HCT 116 a widely used model in colorectal cancer research, particularly for studying oncogenic signaling, DNA mismatch repair deficiency, and tumor suppressor gene regulation. The epithelial origin and well-characterized growth properties support reproducible in vitro experimentation.
EED encodes a core subunit of PRC2 required for the methyltransferase activity of EZH2/EZH1. Along with SUZ12 and RBBP4/RBBP7, EED facilitates H3K27me3 deposition, silencing developmental regulators such as HOX clusters and CDKN2A. PRC2 is regulated by JARID2, AEBP2, PHF1, and HOTAIR. EED knockout disrupts this complex, causes loss of H3K27me3, and derepresses target genes.
In HCT 116 cells, EED disruption allows dissection of PRC2-mediated epigenetic regulation in colorectal cancer. Loss of PRC2 function alters proliferation, differentiation, and drug sensitivity. This model is valuable for investigating how aberrant H3K27me3 contributes to oncogenic gene expression and for studying PRC2 dysregulation in cancers and developmental disorders like Weaver syndrome.
Applications include functional genomics, drug target validation, and epigenetic studies. Typical assays include western blotting (EED, EZH2, H3K27me3), RT?qPCR, ChIP?seq, immunofluorescence, and proliferation assays with EZH2 inhibitors. For further details, contact Ascent Research.
