EHMT1 Knockout NCI-H1299 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human non-small cell lung carcinoma (NSCLC) line NCI-H1299, featuring disruption of the EHMT1 gene. This heterogeneous pool, produced by CRISPR/Cas9-mediated gene targeting, avoids clonal selection bias and is suited for population-level functional genomics studies, drug screening, and pooled molecular analyses. The product provides a loss-of-function model for EHMT1, enabling investigation of its roles in epigenetic silencing without the limitations of single-cell clones.
The parental NCI-H1299 cell line originates from a metastatic lymph node of a lung adenocarcinoma patient and harbors an oncogenic KRAS G12C mutation along with a homozygous deletion of TP53. These genetic features render it an aggressive, widely used model for NSCLC, particularly relevant to study signaling and epigenetic mechanisms in the absence of p53 tumor suppression. Its epithelial morphology supports assays of cell adhesion, migration, and invasion.
EHMT1 is a histone-lysine N-methyltransferase that catalyzes mono- and dimethylation of histone H3 lysine 9 (H3K9me1/2), chromatin marks recognized by HP1 proteins to mediate transcriptional repression. It functions as part of a multimeric complex with EHMT2/G9a, WDR5, and UHRF1, and is regulated by upstream factors including the NOTCH intracellular domain (NICD), CDK2, and the transcription factor SNAI1. Downstream, EHMT1 silences key targets such as CDH1 (E-cadherin) and other tumor suppressor genes, thereby influencing cell adhesion and epithelial-mesenchymal transition. Cross-talk with DNA methylation through DNMT1 further reinforces long-term gene silencing.
In the NCI-H1299 context, EHMT1-dependent H3K9 methylation likely contributes to aberrant silencing of growth-suppressive genes, promoting the oncogenic phenotype. Disruption of EHMT1 in these KRAS-driven, TP53-null cells may relieve such repression, offering a model to study epigenetic reactivation and its impact on proliferation, metastasis, and drug sensitivity. The polyclonal population therefore represents a valuable tool for exploring EHMT1 function in NSCLC and for evaluating H3K9 methyltransferase inhibitors.
Typical applications encompass epigenetic regulation studies, cancer cell proliferation and metastasis assays, and target validation for H3K9 methyltransferases. Compatible assays include Western blotting, RT-qPCR, Sanger sequencing with ICE analysis, ChIP-qPCR for H3K9me2, immunofluorescence, cell migration/invasion assays, and cell viability measurements. The polyclonal format enables robust pooled analysis. For additional information or custom inquiries, please contact Ascent Research.
