The CBX6 Knockout NCI-H1299 Polyclonal Cells are a CRISPR/Cas9-engineered polyclonal knockout population derived from the NCI-H1299 human lung adenocarcinoma epithelial cell line, with targeted disruption of the CBX6 gene. This product provides a heterogeneous pool of edited cells harboring diverse loss-of-function mutations, enabling robust assessment of gene function while avoiding clonal selection bias. The polyclonal format is ideal for bulk population studies and pooled assays requiring averaging of multiple knockout genotypes. Gene editing efficiency is verified by population-level analysis, and the cells are supplied as a ready-to-use research tool for chromatin biology and lung cancer investigations.
NCI-H1299 is an epithelial cell line established from a lymph node metastasis of a non-small cell lung cancer patient. It is widely employed as a model of lung adenocarcinoma, retaining key genomic features such as TP53 mutation and lacking common EGFR mutations. This background makes it a versatile host for studying tumor suppressors, oncogenes, and epigenetic regulators in a metastatic context. The aggressive behavior of NCI-H1299 cells renders them especially useful for investigating genes controlling proliferation, migration, and invasion in advanced lung cancer.
CBX6 functions as a transcriptional repressor and a core subunit of the Polycomb repressive complex 1 (PRC1). It binds H3K27me3, a repressive histone mark deposited by PRC2 (EZH2, SUZ12, EED), and recruits BMI1 and RING1B to catalyze H2AK119ub, leading to chromatin compaction and gene silencing. Key targets include CDKN2A and HOX gene clusters. CBX6 interacts with RYBP and other CBX proteins, and its activity is influenced by Wnt and Notch pathways.
In NCI-H1299 lung adenocarcinoma cells, disruption of CBX6 is expected to relieve PRC1-mediated repression at Polycomb target genes, resulting in reactivation of tumor suppressors like CDKN2A. This loss disrupts the canonical PRC1 recruitment mechanism, reducing H2AK119ub levels and allowing transcriptional derepression of genes involved in cell cycle arrest and apoptosis. Consequently, CBX6 knockout cells may exhibit diminished proliferation, increased apoptosis, and reduced migration, offering a system to dissect the contribution of Polycomb-mediated silencing to NSCLC malignancy. This model is also valuable for assessing the therapeutic potential of CBX6 inhibitors.
Researchers can employ this polyclonal CBX6 knockout population in a diverse array of experimental setups. Standard validation includes Western blotting to confirm CBX6 protein depletion and RT-qPCR to measure derepression of downstream targets like CDKN2A and HOX genes. Global transcriptomic alterations can be profiled by RNA-seq, while ChIP-qPCR for H3K27me3 and H2AK119ub can map epigenetic changes at specific genomic regions. Functional assays for cell proliferation, migration, and invasion provide quantitative insights into phenotypic effects. These cells are also well-suited for drug target validation studies, such as testing CBX6 inhibitors or combining EZH2 inhibitors. For additional information or technical assistance, please contact Ascent Research.
