The KDM3B knockout HeLa polyclonal cells comprise a CRISPR/Cas9-edited polyclonal cell population with disrupted KDM3B in the HeLa cervical adenocarcinoma line. This heterogeneous pool captures diverse loss-of-function mutations, minimizing clonal bias, and is suited for examining population-level impacts on epigenetic regulation, hormone-dependent signaling, and hypoxia responses. The cells are validated for target-gene disruption and are supplied as a ready-to-use tool for functional genomics and compound screening.
HeLa cells, an immortalized epithelial line derived from cervical adenocarcinoma, contain integrated HPV18 sequences that inactivate p53 and Rb, and exhibit an aneuploid karyotype (70?C90 chromosomes). This transformed background is a classic model for studying oncogenesis, viral carcinogenesis, and drug responses. For KDM3B knockout, it offers a relevant context for investigating epigenetic deregulation in cervical cancer.
KDM3B functions as a critical epigenetic regulator, removing repressive methylation marks from H3K9 to promote open chromatin. It serves as a co-activator for nuclear hormone receptors including AR and ER?? and is transcriptionally upregulated by HIF1A during hypoxia. KDM3B forms complexes with HDAC3, NCoR/SMRT, and the homologous demethylase JMJD1C. Its demethylase activity modulates expression of downstream effectors such as HOXA cluster genes, CCND1, MYC, and TFF1, thereby influencing cell cycle progression, hormone response, and adaptation to low oxygen. The signaling network incorporates upstream inputs from SP1, AR, ER??, and the co-activator EP300, linking chromatin modification to transcriptional outputs in diverse biological contexts.
In HeLa cells, which display constitutive HIF1A activity and altered hormone receptor signaling, KDM3B likely supports aberrant transcriptional programs. CRISPR-mediated KDM3B disruption is expected to impair expression of AR and ER target genes, reduce hypoxia-driven transcriptional responses, and modify chromatin accessibility, thereby compromising proliferation, migration, and drug sensitivity. This knockout model thus provides a system for dissecting KDM3B-dependent oncogenic mechanisms, identifying synthetic lethal interactions, and exploring distinct functions among JmjC domain-containing demethylases.
These cells are suitable for a range of assays. ChIP-qPCR/seq can map H3K9 methylation changes at target loci, while RNA-seq reveals transcriptomic shifts. Protein and mRNA validation via western blotting and RT-qPCR confirms pathway disruption. Functional assays including proliferation, migration, and drug sensitivity testing enable phenotypic characterization. The polyclonal knockout pool also facilitates small-molecule screening to identify compounds exploiting KDM3B loss. For further information, contact Ascent Research.
