KDM5B Knockout Ca Ski Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population in which the KDM5B gene has been disrupted to establish a loss-of-function model. This product is supplied as a heterogeneous pool of cells harboring targeted gene disruption, enabling analysis of KDM5B-dependent epigenetic regulation without clonal selection artifacts. The knockout population is derived from the Ca Ski cell line, providing a physiologically relevant context for functional studies. The product is suitable for short-term phenotypic assays and screening applications, allowing researchers to interrogate KDM5B biology in a flexible and robust cellular system.
The host cell line, Ca Ski, is an adherent epithelial cell line isolated from a cervical epidermoid carcinoma and contains integrated human papillomavirus type 16 (HPV?16) sequences. This line is a widely employed model for cervical cancer research, recapitulating key aspects of HPV-driven oncogenesis, including deregulated cell cycle control and genomic instability. The Ca Ski background provides a well-characterized platform for studying tumor cell biology, drug responses, and the molecular mechanisms underlying cervical carcinoma progression. Its epithelial origin and retention of HPV oncogene expression render it particularly appropriate for investigations into chromatin-based gene regulation in malignant contexts.
KDM5B (JARID1B/PLU-1) encodes a histone demethylase that specifically removes methyl groups from tri- and dimethylated lysine 4 of histone H3 (H3K4me3/me2), thereby acting as a transcriptional repressor. KDM5B is activated by MYC and functions downstream of Notch, TGF???, and E2F transcription factors, while being negatively regulated by miR?137. It directly represses the cyclin-dependent kinase inhibitor p21/CDKN1A and multiple HOX genes, promoting cell cycle progression and inhibiting differentiation. KDM5B interacts with the PRC2 component EZH2, histone deacetylases HDAC1/2, the retinoblastoma protein RB, MYC, and the polymerase?associated factor complex, linking chromatin modification to transcriptional silencing at promoters of genes critical for proliferation and stem cell maintenance.
In the Ca Ski cervical carcinoma background, KDM5B overexpression has been associated with enhanced proliferation, migration, and apoptotic resistance, reflecting its role in maintaining the malignant phenotype. The polyclonal KDM5B knockout population permits dissection of these functions by eliminating target gene activity across a diverse cell pool, thereby averting clone?specific adaptive effects. This model enables investigation of direct KDM5B?dependent chromatin changes and gene expression alterations within a relevant cancer cell milieu, facilitating studies of epigenetic drivers in cervical cancer and providing a comparative platform for other malignancies such as breast, prostate, and acute myeloid leukemia where KDM5B is implicated.
This knockout polyclonal population supports a broad range of applications, including western blotting and RT?qPCR to confirm KDM5B loss and its downstream effects on p21 or HOX gene expression, ChIP?qPCR for H3K4me3 modifications at specific promoters, and functional assays such as MTT proliferation, colony formation, migration/invasion, and annexin V?based apoptosis detection by flow cytometry. Transcriptome analyses via RNA?seq can uncover KDM5B?dependent gene networks. These tools enable detailed investigation of epigenetic regulation, drug sensitivity, and signaling in cervical cancer research. For additional information or technical support, please contact Ascent Research.
