BCL7C Knockout SK-HEP-1 Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal population of SK-HEP-1 human hepatocellular carcinoma cells harboring a disrupted BCL7C gene. This polyclonal pool preserves cellular heterogeneity while establishing a loss-of-function model for studying the tumor suppressor functions of BCL7C. As a ready-to-use resource, it enables reproducible interrogation of BCL7C-dependent phenotypes without the need for single-cell cloning, facilitating robust functional genomics and cancer biology research.
The SK-HEP-1 cell line was established from ascites of a male patient with liver adenocarcinoma and is characterized by co-expression of epithelial and endothelial markers. This dual nature makes it a versatile model for hepatocellular carcinoma biology, including studies of tumor angiogenesis and endothelial-like properties. The line grows reliably in culture and is widely used in signal transduction and oncology research.
BCL7C is a tumor suppressor and integral subunit of the SWI/SNF chromatin remodeling complex, where it directly associates with SMARCA4 (BRG1) and ARID1A. It negatively regulates canonical Wnt/??-catenin signaling by binding ??-catenin and interfering with TCF/LEF transcription factor activity, leading to transcriptional repression of oncogenes such as CCND1 and MYC. The pathway is activated by ligands like WNT3A through FZD/LRP receptors, promoting ??-catenin stabilization and nuclear translocation. BCL7C also modulates apoptosis via BAX and is subject to epigenetic control through promoter DNA methylation, positioning it as a key node in Wnt-driven tumor suppression.
In hepatocellular carcinoma, BCL7C loss frequently occurs and correlates with aberrant Wnt pathway activation and enhanced proliferation. The SK-HEP-1 background, with its mixed lineage features, offers a compelling system to dissect how BCL7C loss affects SWI/SNF-mediated chromatin remodeling and transcriptomic reprogramming. Researchers can apply ChIP-qPCR and RNA-seq to map changes in histone modifications and gene expression, while xenograft studies enable evaluation of tumorigenic potential. This model is particularly useful for investigating synthetic lethality and drug sensitivities, such as to BET inhibitors or Wnt antagonists.
Typical applications include Western blotting and RT-qPCR for target validation (e.g., CCND1, MYC, AXIN2), TOP/FOP flash reporter assays to assess ??-catenin/TCF activity, and EdU or colony formation assays for proliferation. In vivo, the cells can be used in subcutaneous or orthotopic xenograft tumor models in immunodeficient mice. Additional uses encompass drug sensitivity screening, epigenetic inhibitor profiling, and functional genomics approaches. The polyclonal format reduces clonal artifacts and yields robust, reproducible data. For further details, contact Ascent Research.
