The BSG Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the human SK-HEP-1 hepatic adenocarcinoma cell line, featuring targeted disruption of the BSG gene (encoding CD147). This polyclonal knockout pool provides a heterogeneous loss-of-function model that avoids clonal selection artifacts, enabling robust assessment of BSG-dependent cellular processes within a genetically diverse cell background. The cells are shipped as a polyclonal population suitable for immediate expansion and downstream functional analyses.
The SK-HEP-1 parental cell line was originally established from the ascites of a patient with metastatic liver adenocarcinoma and exhibits a unique endothelial-like phenotype alongside its hepatic tumor characteristics. These cells are widely employed to study tumor cell adhesion, transendothelial migration, and the molecular underpinnings of hepatocellular carcinoma invasion. The metastatic origin and plasticity of SK-HEP-1 make it a relevant model system for dissecting late-stage cancer progression pathways.
BSG, also known as CD147 or EMMPRIN, is a multifunctional transmembrane glycoprotein that stimulates the production of matrix metalloproteinases (MMPs), notably MMP-1, MMP-2, MMP-9, and MT1-MMP, while also modulating integrin-mediated adhesion and immune cell interactions. BSG functions upstream of the MAPK/ERK and PI3K/Akt/mTOR cascades, promoting NF-??B activation and subsequent MMP transcription. Upstream signals from EGF, TGF-??, and hypoxia (via HIF-1??) converge on the BSG promoter through transcription factors SP1 and AP-1. BSG also acts as a coreceptor for cyclophilins (Cyclophilin A and B) and interacts with monocarboxylate transporters MCT1 and MCT4, S100A9, Integrin ??1, and Caveolin-1 to coordinate cell surface signaling complexes. Disruption of BSG therefore uncouples these signaling nodes from downstream invasive effectors.
In the SK-HEP-1 context, BSG knockout is expected to significantly attenuate the invasive capacity of these metastatic adenocarcinoma cells by impairing MMP induction and weakening pro-migratory signaling through MAPK/ERK and PI3K/Akt pathways. The endothelial-like properties of SK-HEP-1 further amplify the relevance of BSG depletion, as CD147 is implicated in tumor-endothelial cell interactions and angiogenesis via VEGF upregulation. This model thus serves to dissect the BSG-dependent mechanisms that drive hepatic tumor cell dissemination.
Researchers can employ the BSG Knockout SK-HEP-1 polyclonal cells for applications such as investigating the molecular regulation of cancer invasion and metastasis, screening anti-metastatic compounds, or studying the role of CD147 in SARS-CoV-2 entry, given its documented function as a viral receptor. Typical assays include Transwell invasion and migration assays, gelatin zymography for MMP activity, western blotting and qPCR for signaling component analysis, and phospho-ERK/Akt profiling to map kinase pathway alterations. For additional information or to inquire about custom models, please contact Ascent Research.
