The CBX8 Knockout MES-OV Polyclonal Cells product consists of a polyclonal population of MES-OV cells harboring CRISPR/Cas9-mediated disruption of the CBX8 gene, generating a heterogeneous loss-of-function model for the chromobox protein CBX8. This polyclonal knockout cell population is designed to enable robust interrogation of CBX8-dependent functions in an ovarian endometrioid carcinoma background. The pooled nature of the product preserves genetic diversity while providing reliable gene disruption across the population, making it suitable for a wide range of functional genomics and epigenetic studies.
The MES-OV cell line is derived from a human ovarian endometrioid carcinoma, representing a well-characterized model of epithelial ovarian cancer. It retains key features of the original tumor, including aberrant signaling pathways and epigenetic dysregulation. As an adherent cell line with stable proliferation characteristics, MES-OV is commonly employed for investigating oncogenic mechanisms, drug responses, and tumor suppressor silencing in ovarian cancer research.
CBX8 is a core component of the canonical Polycomb repressive complex 1 (PRC1), functioning as an epigenetic reader that binds H3K27me3 via its chromodomain, a mark deposited by the PRC2 complex (EZH2, SUZ12, EED). This interaction recruits PRC1 to chromatin, where the RING1B/BMI1 catalytic core catalyzes H2AK119 monoubiquitination, leading to chromatin compaction and stable transcriptional repression. Key downstream targets include the tumor suppressors CDKN2A (p16INK4a), CDKN1A (p21), CDH1 (E-cadherin), and HOX gene clusters, placing CBX8 at the intersection of cell cycle control, differentiation, and DNA damage responses.
In ovarian endometrioid carcinoma, CBX8-mediated epigenetic silencing contributes to oncogenic transformation by repressing tumor suppressor genes. This PRC1-dependent mechanism is conserved across multiple malignancies, including breast, liver, and colorectal cancers. The CBX8 knockout MES-OV polyclonal cells enable investigation of how loss of CBX8 affects derepression of these targets and alters cancer cell phenotypes, providing a platform for dissecting polycomb function in tumor progression and metastasis.
Researchers can employ this model for chromatin immunoprecipitation to monitor H3K27me3 occupancy, western blotting of PRC1 components, and RT-qPCR to quantify target gene derepression. Functional readouts such as proliferation, colony formation, and migration assays can be coupled with transcriptomic analyses to profile global changes. This polyclonal knockout population is also suitable for drug sensitivity studies and co-immunoprecipitation of PRC1 complexes. For further technical inquiries or to discuss your experimental needs, please contact Ascent Research.
