The CBX8 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the CBX8 gene in human A2780 ovarian carcinoma cells. This genetically diverse pool provides a robust loss-of-function model free from clonal selection artifacts, enabling faithful assessment of CBX8-dependent phenotypes and epigenetic alterations in a heterogeneous cell context.
The parental A2780 line, derived from an untreated ovarian endometrioid adenocarcinoma, is a widely used epithelial model for ovarian cancer. It retains key tumorigenic features, including altered Polycomb group protein activity, making it an ideal background for investigating CBX8??s contributions to chromatin-mediated transcriptional repression.
CBX8 is a chromodomain-containing subunit of the Polycomb repressive complex 1 (PRC1) that specifically recognizes trimethylated histone H3K27 (H3K27me3). It anchors the RING1B/BMI1 catalytic core to chromatin, promoting monoubiquitination of histone H2A at K119 (H2AK119ub) and subsequent transcriptional repression of targets including the tumor suppressors CDKN2A (p16/INK4a) and CDKN1A (p21). CBX8 activity is regulated upstream by E2F transcription factors and non-coding RNAs such as miR-101, miR-200 family members, and the lncRNA HOTAIR. Within the PRC1 complex, CBX8 interacts with RING1B, BMI1, PCGF2, and PHC1 to couple H3K27me3 recognition with H2AK119ub deposition, thereby maintaining stable gene silencing.
In A2780 ovarian cancer cells, CBX8 overexpression contributes to an epigenetically repressed state at pro-differentiation and tumor-suppressive loci, fostering malignant phenotypes. Knockout of CBX8 in this polyclonal population is anticipated to relieve PRC1-mediated silencing, enabling investigation of CBX8-dependent changes in proliferation, apoptosis, migration, and chemosensitivity. This model is clinically relevant for dissecting epigenetic vulnerabilities in ovarian carcinoma and for evaluating combination therapies targeting Polycomb pathways.
Typical applications include immunoblotting and RT-qPCR to verify knockout and derepression of CDKN2A/p21; ChIP-qPCR for H3K27me3 and H2AK119ub alterations; chromatin accessibility profiling via ATAC-seq and transcriptomic analysis via RNA-seq; and functional phenotyping with proliferation, colony formation, migration, and invasion assays. Drug sensitivity screens, including PARP inhibitor testing, can uncover synthetic lethal interactions. For further product details and custom inquiries, please contact Ascent Research.
