Panoply™ Human BSG Knockdown Stable Cell Line

Name: Panoply™ Human BSG Knockdown Stable Cell Line
SKU: CSC-DC001552
Availability: InStock

For research use only. Not intended for any clinical use.

Cat. No. : CSC-DC001552

Host Cell : HEK293 (Hela and other cell types are also available) Validation : Real-Time RCR

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Cell Line Information

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Gene Information

Cat. No.	CSC-DC001552
Description	Creative Biogene's Knockdown Cell Lines are target specific shRNA lentivirus transduced cells. The percent knockdown levels range from 75-99% depending on the gene, as evaluated by Real-Time RCR. Cells are rigorously qualified and mycoplasma free.
Target Gene	BSG
Host Cell	HEK293 (Hela and other cell types are also available)
Host Cell Species	Homo sapiens (Human)
Applications	(1) Studying gene functions (2) Studying gene interactions and signaling pathways (3) Target validation and drug discovery (4) Designing diseases models
Size	>1 × 10⁶ cells / vial
Stability	Validated for at least 10 passages
Validation	Real-Time RCR
Quality Control	Negative for bacteria, yeast, fungi and mycoplasma.
Storage	Liquid Nitrogen
Shipping	Dry Ice

Mycoplasma	Negative
Format	One frozen vial containing millions of cells
Storage	Liquid nitrogen
Safety Considerations	The following safety precautions should be observed. 1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum. 2. No eating, drinking or smoking while handling the stable line. 3. Wash hands after handling the stable line and before leaving the lab. 4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells. 5. All waste should be considered hazardous. 6. Dispose of all liquid waste after each experiment and treat with bleach.
Ship	Dry ice

Gene Name	BSG basigin (Ok blood group) [ Homo sapiens ]
Gene Symbol	BSG
Synonyms	BSG; basigin (Ok blood group); basigin (OK blood group) , OK; basigin; CD147; EMMPRIN; CD147 antigen; OK blood group antigen; collagenase stimulatory factor; leukocyte activation antigen M6; extracellular matrix metalloproteinase inducer; tumor cell-derived collagenase stimulatory factor; M6; OK; 5F7; TCSF;
GeneID	682
Uni ProtID	P35613
mRNA Refseq	BC009040
Chromosome Location	19p13.3
Function	lactate transmembrane transporter activity; mannose binding; sugar binding;
Pathway	Basigin interactions, organism-specific biosystem; Cell surface interactions at the vascular wall, organism-specific biosystem; Hemostasis, organism-specific biosystem; Integrin cell surface interactions, organism-specific biosystem; Matrix Metalloproteinases, organism-specific biosystem; Metabolism, organism-specific biosystem; Pyruvate metabolism, organism-specific biosystem;
MIM	109480

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Accumulating evidence indicates that solid tumors exhibit features of collective invasion, but the underlying molecular mechanisms remain unclear. Here, researchers aimed to investigate the role of CD147 (also known as BSG or EMMPRIN) in collective invasion in hepatocellular carcinoma (HCC) and its underlying mechanisms. Results indicate that human HCC exhibits collective invasion, with CD147 upregulated at the invasive front of the tumor cell cluster. Using a modified three-dimensional invasion model, researchers confirmed that CD147 promotes collective invasion, recapitulating key features of collective invasion. Transcriptome analysis and enzyme activity assays revealed that CD147 enhances the expression and activity of cathepsin B. Upregulation of cathepsin B in HCC cells promotes cell migration and invasion, thereby mediating the CD147-induced HCC invasive phenotype. Mechanistically, CD147 promotes cathepsin B transcription by activating the β-catenin signaling pathway, while reducing GSK-3β expression. Furthermore, elevated expression of CD147 and cathepsin B correlates with poor prognosis in HCC patients.

Given that CTSB transcription is regulated by β-catenin signaling, researchers investigated whether CD147 regulates β-catenin signaling in hepatocellular carcinoma (HCC). β-catenin is thought to translocate to the nucleus and activate target genes. Here, researchers found that nuclear localization of β-catenin was reduced in CD147 knockdown cells (Figure 1a-b). To confirm these results, they compared the distribution of β-catenin between the nucleus and cytoplasm. Consistent with previous results, nuclear distribution of β-catenin was significantly reduced upon CD147 knockdown (Figure 1c-d). In CD147 knockdown Huh-7 and HepG2 cells, TOP/FOP transcriptional activity was significantly attenuated (Figure 1e), indicating that CD147 knockdown attenuates β-catenin signaling. Mechanistically, CD147 knockdown enhanced the expression of GSK-3β, a component of the β-catenin destruction complex (Figure 1f-g), while CD147 overexpression had the opposite effect (Figure 1h-i). These results suggest that CD147 may activate the β-catenin signaling pathway by inhibiting the expression of GSK-3β.

Figure 1. CD147 activates β-catenin signaling via downregulating GSK-3β. (Wang S J, et al., 2020)

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