The KDM2B Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of human SK-HEP-1 hepatic adenocarcinoma cells with targeted disruption of the KDM2B gene. This heterogeneous knockout pool provides a robust loss-of-function model for studying KDM2B-dependent epigenetic regulation without the biases of clonal selection. The product is suitable for investigating the functional consequences of KDM2B ablation in a liver cancer context.
SK-HEP-1 is an established epithelial cell line derived from ascites fluid of a patient with hepatic adenocarcinoma. Widely used in hepatocellular carcinoma research, these cells retain key tumorigenic features, including growth factor responsiveness and invasive properties. The SK-HEP-1 background is an ideal platform to dissect the epigenetic contributions of KDM2B to liver cancer biology, particularly in the context of signaling pathways implicated in tumor progression.
KDM2B encodes a JmjC histone demethylase targeting H3K36me2/me1, with affinity for H3K4me3, repressing transcription. It complexes with BCOR, PCGF1, HP1, and HDAC1/2. KDM2B integrates MYC, ??-catenin/TCF, and TGF-??/SMAD (SMAD2/3, SMAD4) signals. It silences CDKN1A (p21) and CDKN2A (p16), while regulating CCND1, CDH1, rRNA, and telomere genes. mTOR modulation involves S6K and 4E-BP1. Knockout abrogates H3K36me2/me1 demethylation, derepresses targets, causing cell cycle arrest, impaired EMT, and heightened apoptosis.
In the SK-HEP-1 hepatocellular carcinoma context, KDM2B knockout reactivates p21 and p16, triggering G1/S arrest and reduced proliferation, mirroring a potential anti-cancer mechanism. Loss of KDM2B also blunts TGF-??-induced EMT, underscoring its role in metastatic programs. This model enables dissection of epigenetic crosstalk with Wnt/??-catenin (involving ??-catenin and TCF4) and mTOR cascades. The polyclonal knockout population captures heterogeneous editing outcomes, reflecting tumor cell diversity and allowing robust drug response studies without clonal artifacts.
Researchers can utilize this knockout model to study epigenetic regulation in hepatocellular carcinoma, KDM2B-dependent cell cycle and apoptosis, and TGF-??-induced EMT. It is suited for drug screening of KDM2B inhibitors and functional genomics. Compatible assays include western blotting, RT-qPCR, ChIP-qPCR, viability/apoptosis analyses, Transwell migration/invasion, colony formation, and RNA-seq. For further technical details or to order, please contact Ascent Research.
