The KDM1B Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout pool generated from the human SK-HEP-1 hepatic adenocarcinoma cell line. This population carries heterogeneous disruption of the KDM1B gene, which encodes a histone lysine demethylase critical for epigenetic regulation. The polyclonal format captures the diversity of editing outcomes, providing a robust loss-of-function model without the need for single-cell cloning. It is suitable for functional genomics, drug screening, and mechanistic studies in hepatocellular carcinoma.
SK-HEP-1 cells were originally derived from the ascitic fluid of a patient with liver adenocarcinoma. They exhibit endothelial-like characteristics and are widely used as a model of hepatocellular carcinoma (HCC). This cell line is valuable for investigating tumor progression, metastasis, and signaling pathways relevant to HCC, particularly those involving epithelial-to-mesenchymal transition (EMT). Its unique phenotype allows exploration of both hepatic and endothelial aspects of cancer biology.
KDM1B (also known as LSD2) is a histone lysine demethylase that specifically removes mono- and dimethyl marks from histone H3 at lysine 4 (H3K4me1/2). As a transcriptional corepressor, it forms complexes with GLYR1 (NPAC) and histone deacetylases HDAC1/HDAC2. KDM1B is regulated by E2F transcription factors and downstream targets include the tumor suppressors CDKN1A (p21) and TP53, the pro-apoptotic factor BAX, and the epithelial?Cmesenchymal markers CDH1 (E-cadherin) and VIM (vimentin). Via its demethylase activity, KDM1B influences TGF-??/TGFBR1/SMAD2/3 and Wnt/Frizzled/??-catenin/TCF signaling, thereby modulating cell proliferation, apoptosis, and differentiation.
In SK-HEP-1 cells, KDM1B loss eliminates H3K4me1/2 demethylation, leading to increased methylation at target gene promoters and derepression of tumor suppressors such as CDKN1A and BAX. This alteration disrupts epigenetic silencing of TGF-?? and Wnt pathways, providing a model to study KDM1B’s tumor-suppressive roles in HCC. The knockout also impacts EMT and metastasis mechanisms, as KDM1B normally represses CDH1 and activates VIM. With its combined hepatic and endothelial traits, SK-HEP-1 enables analysis of how KDM1B influences both cancer cell-intrinsic and microenvironmental properties.
This polyclonal KDM1B knockout model is applicable to a broad range of research applications. It supports functional characterization of KDM1B using ChIP-qPCR for histone methylation, RT-qPCR and Western blotting for target validation, flow cytometry for apoptosis, and Transwell assays for migration. The pool is ideal for high-throughput screening of epigenetic modulators and RNA-seq transcriptomic profiling. Its polyclonal nature ensures robust phenotypic representation, minimizing clonal artifacts. For further information, please contact Ascent Research.
