The KMT2A Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-generated polyclonal cell population featuring disruption of the KMT2A gene within the human SK-HEP-1 liver adenocarcinoma cell line. This product comprises a heterogeneous pool of edited cells with targeted KMT2A ablation, enabling loss-of-function studies without single-cell cloning. It is suited for bulk molecular and phenotypic analyses in a hepatic cancer context.
The host cell line SK-HEP-1 was established from ascites of a patient with liver adenocarcinoma and displays an adherent, epithelial-like morphology. Widely used in hepatocellular carcinoma research, SK-HEP-1 cells retain key oncogenic signaling pathways, including WNT and TGF-??, which intersect with KMT2A-dependent transcriptional regulation.
KMT2A encodes a histone methyltransferase that catalyzes mono-, di-, and trimethylation of histone H3 at lysine 4 (H3K4), a mark of active promoters. It functions within a core complex containing WDR5, RBBP5, ASH2L, and DPY30, and is regulated by upstream TASP1-mediated cleavage and assembly with MEN1/WDR5. KMT2A activity is linked to WNT signaling via interaction with CTNNB1 and TCF/LEF transcription factors. Downstream, KMT2A directly promotes expression of the HOXA and HOXB gene clusters, MEIS1, and cell cycle and apoptosis regulators such as CDKN1A, CDKN2B, CCND1, and BCL2. It also intersects with TGF-?? signaling through SMAD2/3 and collaborates with transcriptional coactivators CREBBP/EP300 and tumor suppressor TP53.
In SK-HEP-1 liver adenocarcinoma cells, KMT2A disruption is expected to alter H3K4 methylation patterns and transcriptional programs governed by this epigenetic writer. Given its control over HOX genes and proliferation/apoptosis mediators, the knockout model enables dissection of KMT2A??s role in hepatic tumor cell growth, survival, and migration. This polyclonal population provides a reproducible system for investigating KMT2A loss-of-function in a solid tumor background relevant to hepatocellular carcinoma.
Researchers can apply this knockout model to study epigenetic dysregulation in liver cancer, validate KMT2A downstream targets, and develop or screen KMT2A-directed therapeutics. Typical assays include western blotting for knockout confirmation, ChIP-qPCR for H3K4 methylation, RT-qPCR for HOX gene expression, and RNA-seq for transcriptome-wide effects. Phenotypic readouts such as MTT proliferation assays, Annexin V apoptosis detection, and Transwell migration/invasion assays are directly applicable. For additional details or technical assistance, please contact Ascent Research.
