The KDM5B Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human SK-HEP-1 hepatic adenocarcinoma line. Engineered for loss-of-function of the KDM5B gene, this polyclonal pool provides a heterogeneous genetic background that avoids clonal biases. It serves as a robust model for studying KDM5B-dependent epigenetic processes in liver cancer.
SK-HEP-1 cells originate from the ascitic fluid of a Caucasian male with liver adenocarcinoma and exhibit a unique dual epithelial-endothelial phenotype. This characteristic makes them a well-established model for hepatocellular carcinoma and endothelial-mesenchymal transition (EMT) investigations. The cell line??s mixed differentiation state is ideal for exploring how epigenetic regulators like KDM5B influence cellular plasticity.
KDM5B (JARID1B) is a histone H3K4me2/me3 demethylase that represses transcription by removing activating chromatin marks. Its expression is upregulated by c-MYC and HIF1?? and is regulated by retinoic acid signaling and miR-137. KDM5B forms complexes with HDAC1/2, NuRD, and PRC2 components, and cooperates with RB1 to silence tumor suppressors, including CDKN1A (p21), p16INK4a, CDH1, and KRT19. This epigenetic silencing promotes stem cell-like properties and contributes to chemoresistance and tumor progression.
In SK-HEP-1 liver cancer cells, KDM5B overexpression drives stemness and resistance to sorafenib. KDM5B knockout in this polyclonal population enables researchers to investigate the reversal of these phenotypes. Loss of KDM5B may reactivate key tumor suppressors, reduce epithelial-to-endothelial transition, and restore drug sensitivity, making this model highly relevant for studying hepatocellular carcinoma biology and identifying therapeutic vulnerabilities.
Applications include epigenetic tumorigenesis studies, KDM5B inhibitor screening, and investigation of hepatocellular carcinoma stem cell mechanisms. Compatible assays feature ChIP-qPCR for H3K4me3 levels, western blotting for histone demethylation, RT-qPCR of targets such as p21 and KRT19, apoptosis and viability analyses, colony formation, migration/invasion assays, and drug sensitivity testing with sorafenib. Flow cytometry for CD133 and CD44 is also supported. For further details, please contact Ascent Research.
