The KDM3B Knockout SK-HEP-1 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human hepatic adenocarcinoma cell line. This loss-of-function model features targeted disruption of the KDM3B gene (encoding lysine demethylase 3B) across a heterogeneous cell pool, enabling robust investigation of KDM3B-dependent epigenetic regulation in liver cancer biology. The polyclonal format preserves a natural spectrum of editing outcomes, avoiding the clonal artifacts associated with single-cell isolation while providing a powerful tool for studying endogenous tumor suppressor functions.
The host SK-HEP-1 cell line was originally established from the ascitic fluid of a patient diagnosed with liver adenocarcinoma and serves as a widely accepted hepatocellular carcinoma model. These adherent epithelial cells exhibit characteristic features of hepatic malignancy, including dysregulated proliferation, resistance to apoptosis, and migratory capacity. As a well-characterized cancer cell line, SK-HEP-1 provides a physiologically relevant context in which to dissect the role of KDM3B in liver tumorigenesis and evaluate the consequences of its inactivation on disease-relevant phenotypes.
KDM3B functions as a histone demethylase that specifically removes mono- and dimethyl marks from lysine 9 on histone H3 (H3K9me1/me2), thereby relieving transcriptional repression at target gene promoters. It is transcriptionally activated by p53 and participates in a signaling axis where p53 induces KDM3B expression, which subsequently demethylates H3K9 at promoters of key downstream targets including CDKN1A (p21), BAX, PUMA, and CDH1 (E-cadherin). This promotes expression of cell cycle inhibitors and pro-apoptotic factors while simultaneously reinforcing epithelial characteristics, directly counteracting oncogenic transformation. Conversely, loss of KDM3B leads to accumulation of repressive H3K9me marks and silencing of these tumor-suppressive genes, resulting in enhanced proliferation, evasion of apoptosis, and epithelial-mesenchymal transition (EMT).
In the SK-HEP-1 background, disruption of KDM3B is predicted to exacerbate the malignant phenotype by removing a critical epigenetic barrier to tumor progression. Without KDM3B-mediated demethylation, p53-responsive apoptotic programs and cell cycle checkpoints become compromised, mirroring events observed in advanced hepatocellular carcinoma where KDM3B is frequently downregulated. This model therefore provides a unique platform to interrogate how loss of this demethylase reshapes the chromatin landscape and transcriptome, driving hallmarks of cancer such as sustained proliferative signaling, resistance to cell death, and activation of invasive programs. It is particularly valuable for delineating the interplay between p53 activity, epigenetic regulation, and liver tumor biology.
The KDM3B Knockout SK-HEP-1 Polyclonal Cells are ideally suited for a broad range of functional oncology and epigenetic research applications. Users can confirm target disruption and monitor global H3K9 methylation changes via Western blotting, while RT-qPCR and RNA-seq enable transcriptional profiling of p21, BAX, and E-cadherin to assess pathway activity. Functional assays such as cell proliferation, apoptosis, and migration/invasion studies directly measure the phenotypic consequences of KDM3B loss, and chromatin immunoprecipitation coupled with qPCR (ChIP-qPCR) permits locus-specific analysis of H3K9me occupancy at gene promoters. These applications support mechanistic studies, drug target validation, and screening for modulators that restore KDM3B-like activity. For more information or to discuss custom requirements, please contact Ascent Research.
