The KDM5B Knockout SK-OV-3 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human ovarian adenocarcinoma cell line SK-OV-3, in which the KDM5B gene has been disrupted to eliminate protein expression. This polyclonal format enables loss-of-function studies without clonal selection, preserving population-level heterogeneity and making the cells suitable for large-scale functional genomics, epigenetic research, and drug screening applications.
The parental SK-OV-3 cell line, established from the ascites of a patient with progressive ovarian adenocarcinoma, is an adherent epithelial model extensively used in cancer research. These cells harbor genomic alterations and signaling aberrations typical of high-grade serous ovarian carcinoma, providing a clinically relevant context for probing the role of the histone demethylase KDM5B in tumor biology.
KDM5B (also known as JARID1B or PLU-1) is a histone H3 lysine 4 demethylase that specifically removes di- and trimethyl marks from histone H3K4 at gene promoters, thereby mediating transcriptional repression. This enzyme is transcriptionally activated by oncogenic MYC and E2F transcription factors and is post-transcriptionally regulated by the tumor suppressor microRNA miR-137. KDM5B functions within multimeric repressor complexes, interacting directly with components of the polycomb repressive complex 2 (PRC2), histone deacetylases HDAC1 and HDAC2, and the nucleosome remodeling and deacetylase (NuRD) complex. Through these interactions, KDM5B targets and demethylates H3K4me2/3 at the promoters of key tumor suppressor genes, including CDKN1A (p21), E-cadherin (CDH1), and HOX family members, leading to their stable silencing. CRISPR/Cas9-mediated disruption of KDM5B is therefore expected to result in elevated H3K4 methylation at these loci, transcriptional reactivation of the repressed genes, and reversal of the oncogenic epigenetic landscape.
In SK-OV-3 ovarian cancer cells, KDM5B is frequently overexpressed and contributes to the aggressive, mesenchymal phenotype through sustained suppression of tumor suppressor loci. Knockout of KDM5B is anticipated to derepress CDKN1A/p21 and E-cadherin, leading to increased protein levels that may promote cell cycle arrest and enhance cell-cell adhesion, while also attenuating migratory and invasive capacity. This polyclonal knockout model thus provides a powerful tool for investigating the direct consequences of KDM5B loss in an ovarian cancer context, enabling dissection of the epigenetic mechanisms underlying tumor progression and assessment of the therapeutic potential of KDM5B inhibition.
This product is well suited for a broad range of experimental applications, including functional genomics of chromatin modifiers, validation of KDM5B as a cancer drug target, and mechanistic studies of epigenetic gene silencing. Researchers can employ these cells in Western blotting to assess global H3K4me3 changes, ChIP-qPCR to examine occupancy at specific target gene promoters, cell proliferation and viability assays, migration and invasion assays, and drug sensitivity profiling. For additional technical information or to place an order, please contact Ascent Research.
