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-SC014507
Host Cell : HEK293 (CHO and other cell types are also available) Size : >1x106 frozen cells/vial
| Cat. No. | CSC-SC014507 |
| 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. |
| Target Gene | SLC34A2 |
| Gene Species | Homo sapiens (Human) |
| Host Cell | HEK293 (CHO and other cell types are also available) |
| Host Cell Species | Species varies |
| Applications |
1. Gene expression studies 2. Signaling pathway research 3. Drug screening and toxicology 4. Disease research |
| Size | 2 × 10^6 cells / vial |
| Stability | Validated for at least 10 passages |
| Quality Control | Negative for bacteria, yeast, fungi and mycoplasma. |
| Storage | Liquid nitrogen |
| Shipping | Dry Ice |
| 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. |
| 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 | SLC34A2 solute carrier family 34 (sodium phosphate), member 2 [ Homo sapiens ] |
| Gene Symbol | SLC34A2 |
| Synonyms | NPTIIb; NAPI-3B; NAPI-IIb |
| Gene Description | solute carrier family 34 (sodium phosphate), member 2 |
| GeneID | 10568 |
| Uni ProtID | O95436 |
| mRNA Refseq | NM_006424.2 |
| Protein Refseq | NP_006415.2 |
| Chromosome Location | 4p15.2 |
| Function | phosphate ion binding; sodium ion binding; sodium-dependent phosphate transmembrane transporter activity; sodium:phosphate symporter activity; |
| Pathway | Mineral absorption, organism-specific biosystem; Mineral absorption, conserved biosystem; SLC-mediated transmembrane transport, organism-specific biosystem; Sodium-coupled phosphate cotransporters, organism-specific biosystem; Transmembrane transport of small molecules, organism-specific biosystem; Transport of inorganic cations/anions and amino acids/oligopeptides, organism-specific biosystem; Type II Na+/Pi cotransporters, organism-specific biosystem; |
| MIM | 604217 |
Solute carrier family 34, member 2 (SLC34A2) has been implicated in the development and progression of various malignancies. However, the clinical significance of SLC34A2 in esophageal squamous cell carcinoma (ESCC) and its underlying molecular mechanisms remain unclear. Here, researchers demonstrate that SLC34A2 expression is significantly upregulated in ESCC and correlates with adverse clinicopathological features (particularly Ki-67 labeling index) and poor prognosis in ESCC patients. Overexpression of SLC34A2 promotes ESCC cell proliferation, while silencing of SLC34A2 has the opposite effect. Furthermore, SLC34A2 induces autophagy, promoting ESCC cell proliferation, whereas inhibition of autophagy inhibits it. Further studies revealed that SLC34A2 interacts with the autophagy-related protein STX17, promoting autophagy and proliferation in ESCC cells by inhibiting STX17 ubiquitination and degradation. These findings suggest that SLC34A2 may serve as a prognostic biomarker for ESCC.
Based on the close relationship between high SLC34A2 expression and elevated Ki-67 labeling, the researchers investigated the effect of SLC34A2 on ESCC cell proliferation. First, they generated SLC34A2-overexpressing KYSE520 and KYSE140 cells (Figure 1a, b). Subsequently, CCK-8, colony formation, and EdU assays demonstrated that SLC34A2 overexpression significantly promoted ESCC cell proliferation (Figure 1c-h). Furthermore, cell cycle distribution analysis revealed a significant decrease in the proportion of cells in the G0/G1 phase and an increase in the proportion of cells in the G2/M phase in SLC34A2-overexpressing cells (Figure 1i, j), indicating that SLC34A2 overexpression accelerates cell cycle progression. Xenograft tumor models further demonstrated that elevated SLC34A2 expression accelerated ESCC cell growth in vivo (Figure 1k). Furthermore, immunohistochemical staining showed that the Ki-67 proliferation index of SLC34A2-overexpressing tumors was higher than that of control tumors (Figure 1k). Thus, these results confirm that SLC34A2 upregulation promotes the growth of esophageal squamous cell carcinoma cells both in vivo and in vitro.
Figure 1. Overexpression of SLC34A2 promotes ESCC cell proliferation in vitro and in vivo. (Xu Y, et al., 2024)
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