The BCL7A Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human hepatic adenocarcinoma cell line. This product provides a heterogeneous pool of cells carrying targeted disruption of the BCL7A gene, enabling loss-of-function studies in a relevant liver cancer background. The polyclonal format does not represent a single-cell clone; rather, it encompasses a mixed population with diverse editing outcomes, suitable for assessing overall gene function without clonal bias.
The SK-HEP-1 cell line is a well-characterized adherent epithelial line originally isolated from the ascites of a patient with hepatic adenocarcinoma. These cells are tumorigenic and serve as a widely used model for liver cancer progression, particularly in studies of invasion, metastasis, and therapeutic response. SK-HEP-1 cells exhibit properties of both hepatic and endothelial lineages, offering a unique system to investigate molecular mechanisms underlying hepatocellular carcinoma and related malignancies.
BCL7A is a tumor suppressor that functions as an integral subunit of the SWI/SNF chromatin remodeling complex, where it interacts with core components such as SMARCA4, SMARCC1, SMARCD1, and ARID1A. It negatively regulates the Wnt signaling pathway by mediating transcriptional repression of key Wnt target genes, including CCND1 and MYC. BCL7A is regulated upstream by Wnt ligands (e.g., Wnt3a) through the FZD7 receptor and ??-catenin, and its expression is subject to p53 modulation and epigenetic silencing via promoter methylation. Downstream, BCL7A influences cell cycle progression and apoptosis by controlling BAX and BCL2 family members, thereby linking chromatin remodeling to tumor-suppressive gene expression programs.
In the SK-HEP-1 context, disruption of BCL7A leads to enhanced Wnt/??-catenin signaling and increased proliferative capacity, recapitulating aspects of hepatocarcinogenesis driven by SWI/SNF complex dysfunction. The polyclonal knockout population allows for investigation of BCL7A-dependent phenotypes such as cell cycle deregulation, resistance to apoptosis, and altered migratory behavior, all relevant to liver tumor biology. This model is particularly valuable for studying the interplay between chromatin remodeling and oncogenic signaling pathways that contribute to hepatic tumor progression and metastasis.
Research applications include detailed Wnt pathway analysis using Wnt reporter assays and ChIP-qPCR to assess ??-catenin occupancy and target gene expression. The polyclonal cells are suitable for colony formation and transwell migration assays to evaluate proliferative and invasive phenotypes. Additionally, they can be employed in drug sensitivity testing, co-immunoprecipitation studies to probe SWI/SNF complex integrity, and xenograft tumor growth models to assess in vivo tumorigenic potential. For further information or custom orders, please contact Ascent Research.
