The KAT6B Knockout SK-HEP-1 Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal population of human SK-HEP-1 hepatic adenocarcinoma cells harboring a targeted disruption of the KAT6B gene. This loss-of-function model is generated by CRISPR/Cas9-mediated gene disruption, yielding a heterogeneous knockout cell pool suitable for investigating KAT6B-dependent processes without the need for single-cell cloning. The polyclonal format provides a robust system for studying gene function in a population context, minimizing clonal artifacts while maintaining the genetic background of the parental SK-HEP-1 line.
SK-HEP-1 is a well-established human hepatic adenocarcinoma cell line exhibiting both endothelial and epithelial characteristics. Originally derived from ascites of a liver cancer patient, this cell line is widely employed as a model for hepatocellular carcinoma, metastasis, and drug metabolism. Its hybrid phenotype makes it particularly useful for studying epithelial-to-mesenchymal transition and tumor cell plasticity. The SK-HEP-1 line is adherent, rapidly proliferating, and amenable to a range of molecular and cellular techniques, providing a reliable host for knockout studies in liver cancer biology.
KAT6B (also known as MORF or MYST4) is a histone acetyltransferase that catalyzes acetylation of histones H3 and H4, functioning as a transcriptional coactivator within large multiprotein complexes including TRRAP, ING5, EPC1, and BRPF1. It is recruited to chromatin by transcription factors such as the NICD/RBP-J complex, where it acetylates histone H3 at target gene promoters to activate transcription of downstream effectors like HES1. KAT6B integrates signals from Notch, Wnt, and p53 pathways, and its activity is regulated by NICD, p53, and cell cycle cues. Through HES1 and p21 (CDKN1A), KAT6B influences cell proliferation, differentiation, and survival, with additional roles in HOX gene expression and hematopoietic development.
In hepatocellular carcinoma, aberrant KAT6B expression has been linked to oncogenic signaling and tumor progression. The SK-HEP-1 model, with its intrinsic liver cancer properties, allows dissection of KAT6B contributions to proliferation, migration, invasion, and drug sensitivity. By disrupting KAT6B in this context, researchers can examine its role in Notch pathway hyperactivity, p53-mediated responses, and chromatin remodeling events that drive malignancy. This knockout model is particularly valuable for studying epigenetic mechanisms underlying sorafenib resistance and for identifying KAT6B-dependent vulnerabilities in liver cancer cells.
This polyclonal knockout cell population is suitable for a broad range of functional assays, including Western blotting for KAT6B protein expression, RT-qPCR analysis of downstream targets such as HES1 and p21, ChIP-qPCR to assess histone H3 acetylation at target promoters, proliferation and migration/invasion assays, and drug sensitivity testing with agents like sorafenib. It also supports Notch reporter assays and chromatin modification studies. Researchers can employ this model to explore epigenetic regulation, oncogenic signaling, and therapeutic resistance mechanisms. For additional technical details or custom inquiries, please contact Ascent Research.
