Transfected Stable Cell Lines
Reliable | High-Performance | Wide Rage
Precision reporter, kinase, immune receptor, biosimilar, Cas9, and knockout stable cell lines for diverse applications.
Cat. No. : CSC-DC000388
Host Cell : HEK293 (Hela and other cell types are also available) Validation : Real-Time RCR
| 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; |
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. (Sun S, et al., 2019)
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