Cat.No. : CSC-SC005162 Host Cell: HEK293 (CHO and other cell types are also available)
| Cat. No. | CSC-SC005162 |
| 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 | EZH2 |
| 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 | EZH2 enhancer of zeste homolog 2 (Drosophila) [ Homo sapiens ] |
| Gene Symbol | EZH2 |
| Synonyms | ENX1; EZH1; KMT6; WVS2; ENX-1; KMT6A |
| Gene Description | enhancer of zeste homolog 2 (Drosophila) |
| Gene ID | 2146 |
| UniProt ID | Q15910 |
| mRNA Refseq | NM_001203249.1 |
| Protein Refseq | NP_001190178.1 |
| Chromosome Location | 7q35-q36 |
| Function | DNA binding; chromatin binding; core promoter binding; histone methyltransferase activity; histone-lysine N-methyltransferase activity; protein binding; sequence-specific DNA binding; |
| Pathway | Integrated Pancreatic Cancer Pathway, organism-specific biosystem; miRs in Muscle Cell Differentiation, organism-specific biosystem; |
| MIM | 601573 |
| 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 |
The impact of the oncogene Ezh2 on gastric cancer (GC) progression and prognosis, and its underlying mechanisms, remain unclear. Here, researchers investigated the clinicopathological significance of Ezh2 in gastric cancer and its role in gastric cancer development and progression. Ezh2 expression levels were higher in gastric cancer tissues compared to adjacent non-tumor epithelial tissues. High Ezh2 expression was associated with more aggressive biological behavior and poor prognosis in gastric cancer. In vitro studies showed that Ezh2 promoted gastric cancer cell proliferation and colony formation. Furthermore, Ezh2 induced gastric cancer cells to acquire an epithelial-mesenchymal transition (EMT) phenotype and enhanced their migration and invasion capabilities. Notably, Ezh2 enhanced the spheroid formation ability of gastric cancer cells, suggesting its role in enriching gastric cancer stem cells. In addition, researchers found that the PTEN/Akt signaling pathway was involved in the effects of Ezh2 on gastric cancer cell stem cell characteristics and EMT phenotype, and blocking the PTEN signaling pathway significantly reversed the effects of Ezh2. In summary, Ezh2 plays a crucial role in multiple aspects of gastric cancer pathogenesis, partly through the PTEN/Akt signaling pathway, suggesting that Ezh2 may be an independent prognostic factor and a potential therapeutic target.
To further investigate the biological function of Ezh2 in gastric cancer, researchers measured the basal expression levels of Ezh2 in five gastric cancer cell lines and compared them with a normal human gastric mucosal cell line (GES-1). The results showed that the expression level of Ezh2 in gastric cancer cells was significantly higher than that in GES-1 cells (Figure 1a). Based on the basal expression levels of Ezh2, the researchers selected MKN-45 and SGC-7901 gastric cancer cell lines for Ezh2 overexpression and the AGS cell line for Ezh2 gene knockdown. Western blotting experiments confirmed the efficiency of overexpression and gene knockdown (Figure 1a). The study showed that the in vitro proliferation rate of Ezh2-overexpressing cells was significantly higher than that of control cells (Figure 1b), while Ezh2 knockdown inhibited the proliferation of AGS cells, which was confirmed in both CCK-8 assays (Figure 1b) and colony formation assays (Figure 1c). Furthermore, a mouse xenograft model showed that the tumor volume formed by Ezh2 knockdown cells in nude mice was smaller than that of the control group. Consistent with the previously reported role of Ezh2 in promoting tumor growth, these results indicate that Ezh2 can promote tumor growth (Figure 1d).
Figure 1. Ezh2 promotes GC cell proliferation, clonogenicity, invasiveness and sphere-forming capacity. (Gan L, et al., 2018)
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