The KMT2C Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the SK-HEP-1 hepatic adenocarcinoma cell line. This heterogeneous pool of cells features targeted disruption of KMT2C, eliminating wild-type function without clonal selection. It provides a ready-to-use model capturing editing diversity, suitable for functional assays in liver cancer that require a mixed genetic background mirroring tumor heterogeneity.
The host cell line, SK-HEP-1, originates from the ascitic fluid of a patient with liver adenocarcinoma and is widely employed as a model for hepatocellular carcinoma. SK-HEP-1 cells exhibit characteristics of hepatic adenocarcinoma, including anchorage-independent growth and tumorigenic potential in xenograft models. Their molecular profile includes expression of epithelial and mesenchymal markers, making them valuable for studying cancer cell plasticity and metastasis. This cell line has been extensively characterized in liver cancer research, providing a well-defined platform for investigating the role of epigenetic regulators in hepatocarcinogenesis.
KMT2C encodes a histone methyltransferase that catalyzes mono-, di-, and trimethylation of histone H3 at lysine 4 (H3K4), a mark associated with active transcription. KMT2C functions within the COMPASS complex, interacting with cofactors such as UTX (KDM6A), PTIP, PA1, NCOA6, and ASC-2 to regulate chromatin structure. Its catalytic activity is modulated by Wnt signaling: upon pathway activation, ??-catenin translocates to the nucleus and associates with TCF/LEF transcription factors, including TCF4, to recruit KMT2C to target gene promoters. This recruitment leads to H3K4me3 deposition and transcriptional activation of downstream effectors such as HOX gene clusters and genes controlling proliferation and differentiation. Thus, KMT2C acts as a key epigenetic coactivator linking Wnt signals to gene expression programs.
Disruption of KMT2C in SK-HEP-1 cells ablates its methyltransferase activity, resulting in loss of H3K4me3 at target gene promoters and altered chromatin accessibility. This epigenetic remodeling dysregulates transcriptional networks that normally restrain tumor growth, potentially impairing tumor suppressor functions and reshaping the hepatocellular carcinoma phenotype. The knockout model enables dissection of KMT2C-dependent pathways in liver cancer, including its role in maintaining differentiation, controlling cell cycle progression, and modulating response to Wnt signals. By comparing polyclonal knockout cells with wild-type SK-HEP-1, researchers can identify KMT2C-specific contributions to oncogenic processes and evaluate its potential as a therapeutic target.
The KMT2C Knockout SK-HEP-1 Polyclonal Cells are ideal for functional genomics in hepatocellular carcinoma research, enabling mechanistic studies of KMT2C in tumor suppression, epigenetic regulation, and Wnt-driven transcription. Typical assays include Western blotting, RT-qPCR, RNA-seq, and ChIP-seq for H3K4me3 profiling. Functional readouts such as cell viability, colony formation, migration, and drug sensitivity assays elucidate its role in cancer cell behavior and drug response. This polyclonal knockout pool is a valuable resource for chromatin biology, target validation, and preclinical drug discovery. For additional information, please contact Ascent Research.
