BSG Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma cell line, designed for targeted disruption of the BSG gene (also known as CD147). This polyclonal population comprises a heterogeneous mixture of edited cells, providing a robust loss-of-function model for studying BSG-dependent processes without clonal selection bias. The use of CRISPR/Cas9-mediated gene disruption ensures efficient ablation of BSG expression, enabling researchers to dissect its role in a widely used lung cancer background.
A-549 cells are an established model of human alveolar epithelial adenocarcinoma, originally isolated from a 58-year-old Caucasian male. These adherent cells exhibit epithelial morphology and retain numerous characteristics of type II pneumocytes, including the ability to synthesize lecithin and respond to corticosteroids. A-549 cells are extensively utilized in cancer biology, respiratory disease research, and drug testing due to their well-characterized signaling networks and sensitivity to oncogenic stimuli. Their lung adenocarcinoma origin makes them particularly relevant for studying metastatic dissemination, epithelial-mesenchymal transition, and tumor microenvironment interactions.
BSG (CD147/EMMPRIN) is a heavily glycosylated transmembrane protein belonging to the immunoglobulin superfamily. It functions as a primary receptor for extracellular cyclophilins (CyPA and CyPB) and mediates induction of matrix metalloproteinases (MMPs), especially MMP1, MMP2, and MMP9, through activation of NF-??B and MAPK/ERK cascades. BSG forms complexes with monocarboxylate transporters MCT1 and MCT4 and ??1-integrins, facilitating lactate transport and cell adhesion. Its expression is upregulated by TNF-??, TGF-??, EGF, and hypoxia (via HIF-1??), and it transcriptionally regulates downstream effectors including VEGF, hyaluronan synthase, IL-6, and additional TNF-??, establishing auto-regulatory loops. Through these interactions, BSG orchestrates extracellular matrix degradation, cell migration, invasion, and immune modulation.
In A-549 cells, BSG is highly expressed and contributes to the invasive phenotype characteristic of lung adenocarcinoma. Disruption of BSG in this polyclonal knockout model is expected to significantly attenuate MMP production and activity, impair cell migration and invasion in Transwell assays, and potentially alter lactate transport via impaired MCT association. The model also enables investigation of BSG roles in cyclophilin-mediated signaling, caveolin-1 interactions, and downstream PI3K/Akt pathway modulation. Since A-549 cells are permissive to SARS-CoV-2 entry partly via CD147, this knockout resource is also valuable for studying alternative viral entry mechanisms.
This polyclonal knockout cell population is immediately applicable to a range of experimental approaches, including Western blotting for BSG and MMP expression, gelatin zymography for MMP activity, RT-qPCR profiling of MMP genes and inflammatory cytokines, immunofluorescence for BSG localization, and flow cytometry for surface CD147 quantification. Researchers can employ co-immunoprecipitation to examine BSG?CMCT or BSG?Cintegrin interactions and assess lactate transport kinetics. The model supports cancer invasion and metastasis studies, anti-metastatic drug screening, viral entry investigations, and inflammatory disease modeling where BSG-mediated MMP induction is a central pathogenic mechanism. For further technical specifications or to inquire about this product, please contact Ascent Research.
