KDM2B Knockout HeLa Polyclonal Cells from Ascent Research consist of a polyclonal population of HeLa cells with CRISPR/Cas9-mediated disruption of the KDM2B gene. This knockout model provides a loss-of-function system for investigating KDM2B’s roles in chromatin modification and gene regulation. The polyclonal format avoids clonal artifacts and captures the functional diversity of edited cells, making it suitable for a broad range of assays.
HeLa cells are a human epithelial cell line derived from cervical adenocarcinoma and harbor integrated HPV18. As a widely characterized cancer model, HeLa offers rapid proliferation, high transfectability, and extensive molecular annotation. The cervical cancer origin makes this line particularly relevant for studying oncogenic mechanisms, including those influenced by viral oncoproteins and epigenetic regulators like KDM2B.
KDM2B is a JmjC domain histone demethylase specific for H3K36me1/me2. It functions within a non-canonical PRC1 complex, interacting with RING1B, PCGF1, and BCOR to repress transcription at CpG island promoters via its CXXC domain. Upstream regulators include the ??-catenin/TCF complex, MYC, E2F1, HIF1A, and TGF-?? signaling. KDM2B’s demethylase activity and scaffolding role lead to silencing of key targets such as the CDKN2A locus (p16INK4a/p14ARF), rDNA repeats, CCND1, and HOX clusters. Additional interacting partners include CXXC1, the SKP1/CUL1/RBX1 E3 ligase, and CTBP2. Through these interactions, KDM2B promotes cell proliferation and inhibits senescence, linking epigenetic modification to cancer progression.
In the HeLa cervical adenocarcinoma context, KDM2B’s function is particularly relevant as its repression of the CDKN2A locus can cooperate with HPV18 E6- and E7-driven degradation of p53 and Rb, respectively. Disruption of KDM2B in these cells is expected to relieve epigenetic silencing of p16INK4a and p14ARF, leading to cellular senescence and proliferation arrest. Consequently, this polyclonal knockout model is a valuable tool for studying the contribution of KDM2B-dependent chromatin regulation to cervical cancer and for evaluating therapeutic strategies targeting histone demethylation.
Typical applications include ChIP-qPCR or ChIP-seq for analyzing H3K36me2 levels and PRC1 complex occupancy at genomic loci, RT-qPCR and RNA-seq for measuring changes in gene expression, and Western blotting or immunofluorescence to verify KDM2B loss and histone modification alterations. Functional studies can utilize MTT/BrdU proliferation assays, senescence-associated ??-galactosidase staining, colony formation, and flow cytometric evaluation of cell cycle and apoptosis (Annexin V/7-AAD). This model is also suitable for screening histone demethylase inhibitors and investigating signaling with Wnt/??-catenin or TGF-??. For more details or to order, please contact Ascent Research.
