Genome-edited Cells
Brain
BSG Knockout U118MG Cell Line is a CRISPR/Cas9-edited human glioblastoma knockout cell line targeting the BSG (CD147) gene. BSG encodes a transmembrane glycoprotein that induces MMP expression and regulates lactate transport via interactions with MCT1/MCT4, playing a critical role in tumor invasion and metabolic adaptation. This product serves as a loss-of-function model for glioblastoma research. The U118MG parental line provides a relevant human glioblastoma multiforme background. Disrupting BSG enables studies on MMP-mediated matrix remodeling, lactate metabolism, immune modulation, and drug resistance. Applications include migration/invasion assays, zymography, co-immunoprecipitation, and inhibitor screening.
Detroit 532
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Rabbit Endometrial Epithelial Cell Medium
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The BSG Knockout U118MG Cell Line is a CRISPR/Cas9-edited knockout cell line designed to disrupt the BSG gene in the U118MG human glioblastoma cell line. This product provides a powerful loss-of-function model to investigate the biological functions of BSG (also known as CD147) and its role in cancer biology, particularly glioblastoma progression.
The parental U118MG cell line originates from a human glioblastoma multiforme tumor, exhibiting an epithelial morphology and serving as a well-established in vitro model for brain cancer research. U118MG cells are widely utilized to study glioblastoma cell growth, invasion, and therapeutic responses, making them an ideal host for targeted gene disruption studies.
BSG encodes a transmembrane glycoprotein that acts as a master regulator of matrix metalloproteinase (MMP) expression and lactate transport. Transcriptionally regulated by HIF-1??, NF-??B, Sp1, TGF-??, and induced by growth factors and cytokines such as EGF, TNF-??, and IL-1??, BSG interacts with cyclophilin A, cyclophilin B, MCT1, MCT4, integrin ??3??1, and caveolin-1. Through these interactions, BSG promotes the expression of MMP-1, MMP-2, MMP-9, and VEGF, thereby facilitating extracellular matrix degradation and angiogenesis. Importantly, BSG mediates lactate shuttling via MCTs, supporting the metabolic plasticity characteristic of aggressive tumors. These functions integrate signaling through NF-??B, PI3K/Akt, and MAPK/ERK pathways.
In the context of glioblastoma, BSG is critically involved in tumor invasion, metabolic adaptation, and immune modulation. BSG-driven MMP secretion contributes to the remodeling of the tumor microenvironment, enabling glioblastoma cell infiltration into surrounding brain tissue. Additionally, BSG’s interaction with MCT1/MCT4 facilitates the efflux of lactate, a key oncometabolite that promotes angiogenesis and immunosuppression. Disruption of BSG in the U118MG background thus provides a pertinent model to dissect these interconnected mechanisms, offering insights into how glioblastoma cells circumvent therapeutic interventions.
Researchers can employ the BSG Knockout U118MG Cell Line to delineate the specific contributions of BSG to glioblastoma invasion, MMP-mediated matrix degradation, metabolic symbiosis, and drug resistance. This knockout cell line is suitable for a variety of functional assays, including gelatin zymography to assess MMP activity, Boyden chamber migration and invasion assays, lactate transport measurements, co-immunoprecipitation for protein interaction studies, and immune-based techniques such as immunofluorescence. It also facilitates high-throughput screening of BSG/CD147 inhibitors and evaluation of chemosensitivity. For further information, please contact Ascent Research.
