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Panoply™ Human AGT Knockdown Stable Cell Line

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

Cat. No. :   CSC-DC000388

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

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Gene Information

Cat. No. CSC-DC000388
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 AGT
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 AGT angiotensinogen (serpin peptidase inhibitor, clade A, member 8) [ Homo sapiens ]
Gene Symbol AGT
Synonyms AGT; angiotensinogen (serpin peptidase inhibitor, clade A, member 8); SERPINA8; angiotensinogen; alpha 1 antiproteinase; antitrypsin; serpin A8; angiotensin I; angiotensin II; pre-angiotensinogen; alpha-1 antiproteinase, antitrypsin; serine (or cysteine) proteinase inhibitor; ANHU;
GeneID 183
Uni ProtID P01019
mRNA Refseq BC011519
Chromosome Location 1q42.2
Function acetyltransferase activator activity; growth factor activity; hormone activity; hormone activity; serine-type endopeptidase inhibitor activity; type 1 angiotensin receptor binding; type 2 angiotensin receptor binding;
Pathway ACE Inhibitor Pathway, organism-specific biosystem; Adipogenesis, organism-specific biosystem; Class A/1 (Rhodopsin-like receptors), organism-specific biosystem; Fatty acid, triacylglycerol, and ketone body metabolism, organism-specific biosystem; G alpha (i) signalling events, organism-specific biosystem; G alpha (q) signalling events, organism-specific biosystem; GPCR downstream signaling, organism-specific biosystem;
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Numerous studies have investigated the significance of high-glucose environments in breast cancer; however, the role of angiotensinogen (AGT) in this process remains unclear. In this study, researchers analyzed the potential pro-tumorigenic effects of a high-glucose environment on breast cancer and elucidated the underlying molecular mechanisms. The results demonstrated that a high-glucose environment promoted the proliferation, viability, and anchorage-independent growth of breast cancer cells; furthermore, high-glucose medium significantly enhanced cell migration and invasion capabilities. Mechanistic studies revealed that a high-glucose environment suppressed AGT expression at both the transcriptional and translational levels; conversely, high levels of AGT significantly inhibited breast cancer cell proliferation and viability while impairing migration and invasion. Most importantly, the exogenous introduction of AGT almost completely abolished the pro-tumorigenic effects induced by the high-glucose environment. This study reveals the pro-tumorigenic nature of high-glucose environments regarding breast cancer cells and confirms that this effect is primarily attributable to the suppression of AGT expression.

Previous studies have confirmed that AGT possesses tumor-suppressive properties in hepatocellular carcinoma, prompting researchers to experimentally investigate whether it exerts similar effects in breast cancer cells. To this end, they first established an MCF-7 cell line with stable AGT overexpression. Real-time quantitative PCR (Figure 1A) and Western blot (Figure 1B) analyses confirmed the successful generation of this AGT-overexpressing cell line. Subsequently, the researchers evaluated the impact of AGT overexpression on cell proliferation, viability, migration, and invasion. Under standard culture conditions, the proliferation of AGT-overexpressing MCF-7 cells was significantly inhibited compared to the control group (Figure 1C). Consistent with its growth-inhibitory effect, MTT assay results further demonstrated that AGT reduced cell viability (Figure 1D). In contrast to the metastasis-promoting effects of a high-glucose environment, the study revealed that the migration (Figure 1E) and invasion (Figure 1F) of AGT-overexpressing MCF-7 cells were significantly suppressed. These findings elucidate the anti-tumor properties of AGT in breast cancer cells and may shed light on the underlying mechanisms by which high-glucose environments promote tumor progression in this disease.

Figure 1. AGT inhibits breast cancer proliferation and metastasis.Figure 1. AGT inhibits breast cancer proliferation and metastasis. (Sun S, et al., 2019)

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