Cat.No. : CSC-SC000232 Host Cell: HEK293 (CHO and other cell types are also available)
| Cat. No. | CSC-SC000232 |
| 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 | ADAM17 |
| 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 | ADAM17 ADAM metallopeptidase domain 17 [ Homo sapiens ] |
| Gene Symbol | ADAM17 |
| Synonyms | CSVP; TACE; NISBD; ADAM18; CD156B |
| Gene Description | ADAM metallopeptidase domain 17 (tumor necrosis factor, alpha, converting enzyme) |
| Gene ID | 6868 |
| UniProt ID | B2RNB2 |
| mRNA Refseq | NM_003183.4 |
| Protein Refseq | NP_003174.3 |
| Chromosome Location | 2p25 |
| Function | PDZ domain binding; SH3 domain binding; integrin binding; interleukin-6 receptor binding; metalloendopeptidase activity; metalloendopeptidase activity; metalloendopeptidase activity; metallopeptidase activity; metallopeptidase activity; metallopeptidase activity; protein binding; zinc ion binding; |
| Pathway | Activated NOTCH1 Transmits Signal to the Nucleus, organism-specific biosystem; Alzheimers disease, organism-specific biosystem; Alzheimers disease, conserved biosystem; Alzheimers Disease, organism-specific biosystem; Cytokine Signaling in Immune system, organism-specific biosystem; Delta-Notch Signaling Pathway, organism-specific biosystem; Disease, organism-specific biosystem; |
| MIM | 603639 |
| 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 |
Rosmarinic acid (RA) is a naturally occurring polyphenol compound with various biological properties, including anticancer effects. Metalloproteinase disintegrin and metalloproteinase 17 (ADAM17) can activate epidermal growth factor receptor (EGFR) ligands and promote tumor progression. Here, researchers investigated whether RA exerts its anticancer effects in melanoma cells by downregulating ADAM17. The results showed that compared to normal cells, RA treatment significantly reduced cell viability, proliferation, migration, and invasion capabilities, melanin content, and the expression of related proteins, including MMP2 and MMP9, in A375 cells. RA increased the proportion of TUNEL-positive cells and the expression of pro-apoptotic proteins, but decreased Bcl-2 expression. RA combined with cisplatin (Cis) treatment enhanced the inhibitory effect of cisplatin on cell viability. RA inhibited the expression of the ADAM17/EGFR/AKT/GSK3β signaling pathway, and the ADAM17 inhibitor (TACE prodomain; TPD) further enhanced this inhibition. Furthermore, ADAM17 overexpression blocked all effects of RA, while TPD treatment produced the opposite effect. In conclusion, RA significantly inhibits the proliferation, migration, and invasion of melanoma cells, but promotes apoptosis.
To verify our hypothesis that RA can downregulate ADAM17 expression and inhibit the EGFR/AKT signaling pathway, thereby suppressing melanoma progression, researchers overexpressed ADAM17 in A375 cells (Figures 1a and 1b). Figure 1c shows that cell proliferation was significantly increased in ADAM17-overexpressing cells, but after combined treatment with TPD in the presence of RA, cell proliferation was significantly reduced, even lower than in cells treated with RA alone. Compared to RA treatment, the migration and invasion abilities of ADAM17-overexpressing cells were also increased, while TPD reduced these cellular functions. Therefore, it can be concluded that ADAM17 overexpression can block, while TPD can enhance, the inhibitory effect of RA on cell migration and invasion (Figures 1d-g). These results indicate that the expression of MMP2 and MMP9, which were inhibited by RA in A375 cells, was significantly restored after ADAM17 overexpression and further reduced after combined treatment with TPD.
Figure 1. ADAM17 overexpression reverses, whereas ADAM17 inhibition enhances the effect of RA on melanoma cells proliferation, migration and invasion. (Huang L, et al., 2021)
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