The BCL10 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human liver adenocarcinoma cell line. This loss-of-function model disrupts BCL10, an adaptor protein essential for NF-kappa-B activation. The polyclonal format provides a heterogeneous pool of gene-disrupted alleles, enabling robust phenotypic assessment without clonal artifacts.
SK-HEP-1 is a human liver adenocarcinoma epithelial cell line established from malignant ascites. With an adherent morphology and aneuploid karyotype, it serves as a model for hepatocellular carcinoma, extensively used in hepatic cancer biology and drug discovery. The line retains key features of liver cancer, including proliferative and invasive capacity, providing a relevant background for studying BCL10 function in a hepatic tumor context.
BCL10 functions as an adaptor in the CARD11?CBCL10?CMALT1 (CBM) complex, transducing signals from TCR/CD3 and BCR to NF-kappa-B. Upon PKC-mediated CARD11 phosphorylation, BCL10 recruits MALT1, activating the IKK complex, which phosphorylates I??B, leading to p65/p50 nuclear translocation. This drives expression of IL-2, IL-6, and TNF. BCL10 interacts with TRAF6, TRAF2, and caspase-9, linking to apoptosis and MAP kinase pathways. The CBM complex is a central mediator of adaptive and innate immune signaling, with dysregulation implicated in lymphomas and autoimmunity.
In hepatocellular carcinoma, NF-kappa-B signaling is frequently hyperactivated, promoting survival, proliferation, and drug resistance. BCL10 may modulate hepatic NF-kappa-B through adaptor functions or microenvironmental cross-talk. Disrupting BCL10 in SK-HEP-1 cells allows dissection of its roles in apoptosis, cytokine production, and inflammatory responses in liver cancer. The association of BCL10 with MALT lymphoma further suggests potential oncogenic mechanisms that can be explored in this epithelial model.
This knockout model enables investigation of NF-kappa-B signaling in HCC, BCL10-dependent proliferation and apoptosis, and drug sensitivity. Typical assays include Western blotting for BCL10 and phospho-IKK/p65, NF-kappa-B luciferase reporters, caspase-3/7 activity, Annexin V apoptosis detection, RT-qPCR for IL-6 and TNF, and flow cytometric p65 translocation analysis. Cell migration and invasion assays can assess metastatic traits. For additional product information, contact Ascent Research.
