Cat.No. : CSC-SC010667 Host Cell: HEK293 (CHO and other cell types are also available)
| Cat. No. | CSC-SC010667 |
| Description | Using Creative Biogene's proprietary lentiviral vectors, we subclone the target gene into lentivector, generate the lentivirus particles, sequentially infect the cell line HEK293 (other cell types are also available according to your requirements), and select the clones constantly expressing target gene at high level. |
| Gene | NT5E |
| Gene Species | Homo sapiens (Human) |
| Host Cell | HEK293 (CHO and other cell types are also available) |
| Stability | Validated for at least 10 passages |
| Application | 1. Gene expression studies 2. Signaling pathway research 3. Drug screening and toxicology 4. Disease research |
| Quality Control | Negative for bacteria, yeast, fungi and mycoplasma. |
| Size Form | 2 × 10^6 cells / vial |
| Shipping | Dry Ice |
| Storage | Liquid nitrogen |
| Revival | Rapidly thaw cells in a 37°C water bath. Transfer contents into a tube containing pre-warmed media. Centrifuge cells and seed into a 25 cm2 flask containing pre-warmed media. |
| Gene Name | NT5E 5-nucleotidase, ecto (CD73) [ Homo sapiens ] |
| Gene Symbol | NT5E |
| Synonyms | NT5E; 5-nucleotidase, ecto (CD73); 5 nucleotidase (CD73) , NT5; 5-nucleotidase; CD73; eN; eNT; 5-NT; ecto-5-nucleotidase; Purine 5-Prime-Nucleotidase; NT; NT5; NTE; E5NT; |
| Gene ID | 4907 |
| UniProt ID | P21589 |
| mRNA Refseq | BC015940 |
| Chromosome Location | 6q14-q21 |
| Function | 5-nucleotidase activity; ferrous iron binding; hydrolase activity, acting on ester bonds; metal ion binding; nucleotide binding; |
| Pathway | HIF-1-alpha transcription factor network, organism-specific biosystem; Metabolic pathways, organism-specific biosystem; Metabolism, organism-specific biosystem; Metabolism of nucleotides, organism-specific biosystem; Nicotinate and nicotinamide metabolism, organism-specific biosystem; Nicotinate and nicotinamide metabolism, conserved biosystem; Purine catabolism, organism-specific biosystem; |
| MIM | 129190 |
| 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 |
Cervical cancer is the third most common cancer in the world. CD73 (also known as NT5E) is involved in the progression of many cancers, but there are no reports on the study of CD73 in cervical cancer. Here, the researchers explored the effects of CD73 overexpression on the growth of cervical cancer in vitro and in vivo and its mechanism. The researchers constructed CD73 overexpressing cervical cancer cells (Hela and SiHa cells). The results showed that CD73 overexpression significantly promoted the proliferation of cervical cancer cells in vitro and tumor growth in vivo. In the CD73 overexpressed cell model and transplanted tumor tissue, the expression levels of EGFR and AKT1 were significantly increased. Knockdown of EGFR and AKT1 inhibited the proliferation of CD73 overexpressing cell models, and its mechanisms included inducing cell apoptosis, increasing the number of cells in the G2/M phase, and reducing the number of cells in the G1 phase. In addition, in CD73 overexpressing cells with EGFR/AKT1 knockdown, the expression levels of cell cycle regulatory molecules CDK2, CDK3, and CDKN1A were significantly increased. These research data indicate that CD73 overexpression promotes the growth of cervical cancer in vitro and in vivo by activating the EGFR/AKT1 pathway.
Previous studies have shown that CD73 overexpression is positively correlated with EGFR and AKT1 expression. Here, the researchers found that the expression of EGFR and AKT1 was increased in CD73-overexpressing cervical cancer cell models and transplanted tumor tissues (Figure 1A-C). To verify the effect of EGFR and AKT1 expression levels on the proliferation of CD73-overexpressing cervical cancer cells, they used si-EGFR and si-AKT1 transient transfection techniques to inhibit the expression of EGFR or AKT1 in CD73-overexpressing Hela cells (HelaCD73) and CD73-overexpressing SiHa cells (SiHaCD73) (Figure 1D, 1E). RTCA experiments showed that knocking down EGFR and AKT1 significantly reduced the proliferation rate of CD73-overexpressing Hela cells and CD73-overexpressing SiHa cells (Figure 1F, 1G). These results suggest that EGFR and AKT1 signals play an important role in the increased proliferation rate of CD73-overexpressing cervical cancer cells.
Figure 1. The effects of EGFR and AKT1 expression in HelaCD73 and SiHaCD73 cells proliferation. (Liu C, et al., 2022)
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