The KDM5D Knockout SK-OV-3 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human SK-OV-3 epithelial ovarian cancer cell line. This product contains a heterogeneous pool of cells with targeted disruption of the KDM5D gene, providing a robust loss-of-function model for studying the role of this histone demethylase in cancer biology. The polyclonal nature of the knockout enables assessment of population-level effects without clonal selection, making it well-suited for bulk biochemical and functional assays that require reproducible representation of diverse editing events.
The SK-OV-3 parental cell line originates from a patient with ovarian adenocarcinoma and harbors a mutation in the TP53 tumor suppressor gene, rendering it resistant to cisplatin-based chemotherapy. This well-characterized cell line is widely used as a model of high-grade serous ovarian cancer and exhibits aggressive growth characteristics in vitro and in vivo. Its TP53-null status influences chromatin dynamics and cell cycle control, establishing a valuable system for evaluating the functional contributions of epigenetic modifiers such as KDM5D.
KDM5D encodes a histone lysine demethylase that specifically removes tri-methylation from lysine 4 of histone H3 (H3K4me3), a chromatin mark associated with active transcription. Through this activity, KDM5D functions as a transcriptional repressor, suppressing the expression of proto-oncogenes including CCND1 (cyclin D1) and MYC (c-Myc). It is regulated upstream by androgen receptor signaling and cell cycle regulators, and it physically interacts with the MLL complex, histone H3, and HDAC1 to coordinate chromatin remodeling and gene silencing. Within the KDM5D-H3K4me3-MYC-CCND1-CDKN1A axis, KDM5D-mediated demethylation promotes cell cycle arrest and may exert tumor-suppressive effects. Disruption of KDM5D alters the chromatin landscape, derepressing MYC and CCND1 and thereby promoting proliferation and tumorigenesis.
Loss of KDM5D in the SK-OV-3 ovarian cancer background provides a powerful tool to dissect the interplay between histone demethylation and the transformed phenotype. Given the TP53-deficient and cisplatin-resistant nature of these cells, KDM5D knockout allows investigation of whether its tumor-suppressive function is dependent on p53 status or chemotherapy resistance mechanisms. The derepression of MYC and CCND1 in this polyclonal knockout population can be used to model oncogene addiction and to test therapeutic vulnerabilities in a setting that mimics advanced ovarian cancer.
This polyclonal knockout cell model is ideally suited for epigenetic regulation studies, tumor suppressor research, and drug target validation. Researchers can employ western blotting and RT-qPCR to confirm altered expression of downstream targets, while ChIP-qPCR assays enable mapping of H3K4me3 changes at MYC and CCND1 loci. Proliferation assays, cell cycle analysis, and invasion assays provide functional readouts of the oncogenic consequences of KDM5D loss. By comparing this knockout population to the parental SK-OV-3 line, users can validate the role of KDM5D in chromatin modification and identify synthetic lethal interactions. For further information or technical support, please contact Ascent Research.
