HMGN5 Knockout SK-HEP-1 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 liver adenocarcinoma epithelial cell line. This product features a targeted disruption of the HMGN5 gene, encoding a nucleosome-binding protein that remodels chromatin and facilitates transcriptional regulation. The polyclonal knockout population contains a heterogeneous collection of edited alleles, providing a robust loss-of-function model without clonal selection artifacts. This configuration is suitable for functional genomic studies where biological effects of HMGN5 ablation are evaluated in a mixed genetic background that mirrors tumor cell heterogeneity.
The host SK-HEP-1 cell line, isolated from ascites of a patient with liver adenocarcinoma, is a widely used in vitro model for hepatocellular carcinoma (HCC). These epithelial cells exhibit deregulated proliferation, migration, and survival pathways characteristic of hepatic cancer. As an adherent cell line, SK-HEP-1 supports standard cell culture and a broad range of functional assays, making it practical for cancer biology. Integrating HMGN5 knockout into this HCC background enables dissection of the gene’s role in liver oncogenesis.
HMGN5 is a non-histone chromosomal protein that binds nucleosomes and decompacts chromatin, facilitating transcription factor access. It is activated by upstream Wnt ligands and ??-catenin, and it transcriptionally regulates downstream targets CCND1, MYC, MMP2, and MMP9. HMGN5-mediated chromatin remodeling influences oncogenic pathways including Wnt/??-catenin, where it collaborates with TCF/LEF factors, as well as PI3K/AKT/mTOR and MAPK/ERK signaling. Loss of HMGN5 disrupts these transcriptional programs, attenuating cell cycle progression, proliferation, and migration. Its interaction with histone H3 and nucleosomes positions HMGN5 as a key integrator of extracellular signals and gene expression in cancer cells.
In SK-HEP-1 cells, HMGN5 knockout provides a physiologically relevant system to study HCC aggressiveness. The disruption reduces Wnt/??-catenin-driven transcription, lowering expression of proliferation-promoting CCND1 and MYC, and suppressing matrix metalloproteinases MMP2 and MMP9 involved in invasion. Consequently, these polyclonal knockout cells model the effects of HMGN5 inhibition on tumor growth and metastasis. This model is particularly valuable for exploring crosstalk between chromatin architecture and signal transduction in liver cancer, revealing epigenetic vulnerabilities.
Researchers can employ this knockout population in diverse applications: western blotting to confirm HMGN5 ablation, MTT assays for proliferation, wound healing assays for migration, RT-qPCR for target gene expression, and ChIP-qPCR for chromatin binding. Additional uses include drug response profiling, functional genomics screens, and epithelial-mesenchymal transition studies. This product serves as a ready-to-use tool for dissecting the HMGN5 regulatory network in hepatocellular carcinoma. For further information, please contact Ascent Research.
