Panoply™ Human VEGFA Knockdown Stable Cell Line

Name: Panoply™ Human VEGFA Knockdown Stable Cell Line
SKU: CSC-DC017263
Availability: InStock

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

Cat. No. : CSC-DC017263

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-DC017263
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	VEGFA
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	VEGFA vascular endothelial growth factor A [ Homo sapiens ]
Gene Symbol	VEGFA
Synonyms	VPF; VEGF; MVCD1
Gene Description	vascular endothelial growth factor A
GeneID	7422
Uni ProtID	P15692
mRNA Refseq	NM_001171630.1
Protein Refseq	NP_001165101.1
Chromosome Location	6p12
Function	cell surface binding; chemoattractant activity; cytokine activity; cytokine activity; extracellular matrix binding; fibronectin binding; growth factor activity; growth factor activity; heparin binding; heparin binding; platelet-derived growth factor receptor binding; protein binding; protein heterodimerization activity; protein homodimerization activity; receptor agonist activity; vascular endothelial growth factor receptor 1 binding; vascular endothelial growth factor receptor 2 binding; vascular endothelial growth factor receptor binding;
Pathway	Angiogenesis, organism-specific biosystem; Bladder cancer, organism-specific biosystem; Bladder cancer, conserved biosystem; Cellular response to hypoxia, organism-specific biosystem; Cellular responses to stress, organism-specific biosystem; Cytokine-cytokine receptor interaction, organism-specific biosystem; Cytokine-cytokine receptor interaction, conserved biosystem;
MIM	192240

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Glioblastoma (GBM) is a malignant astrocytic tumor, and its progression involves the regulation of vascular endothelial growth factor-A (VEGFA). However, the specific mechanisms by which VEGFA regulates GBM progression remain unclear. Here, researchers found that VEGFA is highly expressed in GBM tissues, GBM cells, and exosomes derived from both GBM patients and GBM cells. Silencing VEGFA inhibited cell proliferation, tube formation, migration, and invasion, while promoting apoptosis; furthermore, VEGFA knockdown delayed tumor formation. VEGFA promoted the differentiation of myeloid-derived suppressor cells (MDSCs) and their secretion of TGF-β1 by being packaged into exosomes. Additionally, TGF-β1 knockdown produced effects on the GBM cell phenotype similar to those of VEGFA silencing; in A172 and U251 cells, MDSCs attenuated the effects induced by VEGFA knockdown through the secretion of TGF-β1. These results indicate that VEGFA enhances the tumorigenic properties of GBM cells by promoting MDSC differentiation and TGF-β1 secretion, thereby offering a potential therapeutic target for GBM.

Here, the researchers analyzed the effects of VEGFA silencing on the phenotypes of A172 and U251 cells, including cell proliferation, tube formation, migration, invasion, and apoptosis. VEGFA-knockdown A172 and U251 cell lines were established (Figure 1A). In the VEGFA-knockdown cells, the proportion of cells in the G0/G1 phase increased while the proportion in the S phase decreased (Figure 1B and C), suggesting that VEGFA silencing inhibits cell proliferation. As shown in Figure 1D and E, VEGFA depletion induced apoptosis and inhibited tube formation. Furthermore, the migration and invasion capabilities of the VEGFA-knockdown cells were also suppressed (Figure 1F and G). These data indicate that VEGFA knockdown inhibits the tumorigenic properties of GBM cells.

Figure 1. VEGFA knockdown inhibited proliferation, tube formation, migration and invasion and induced apoptosis of A172 and U251 cells. (Tian Y, et al., 2024)

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