Cat.No. : CSC-SC014305 Host Cell: HEK293 (CHO and other cell types are also available)
| Cat. No. | CSC-SC014305 |
| 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 | SLC10A1 |
| 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 | SLC10A1 solute carrier family 10 (sodium/bile acid cotransporter family), member 1 [ Homo sapiens ] |
| Gene Symbol | SLC10A1 |
| Synonyms | SLC10A1; solute carrier family 10 (sodium/bile acid cotransporter family), member 1; sodium/bile acid cotransporter; NTCP; growth-inhibiting protein 29; Na(+)/bile acid cotransporter; sodium/taurocholate cotransporter; solute carrier family 10 member 1; Na(+)/taurocholate transport protein; cell growth-inhibiting gene 29 protein; Na/taurocholate cotransporting polypeptide; sodium/taurocholate cotransporting polypeptide; |
| Gene ID | 6554 |
| UniProt ID | Q14973 |
| mRNA Refseq | BC069799 |
| Chromosome Location | 14q24 |
| Function | bile acid:sodium symporter activity; symporter activity; |
| Pathway | Bile acid and bile salt metabolism, organism-specific biosystem; Bile secretion, organism-specific biosystem; Bile secretion, conserved biosystem; Metabolism, organism-specific biosystem; Metabolism of lipids and lipoproteins, organism-specific biosystem; Recycling of bile acids and salts, organism-specific biosystem; |
| MIM | 182396 |
| 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 |
Hepatocellular carcinoma (HCC) is a highly prevalent and malignant cancer. SLC10A1, a member of solute carrier family 10 (SLC10), is expressed at lower levels in HCC tissues than in adjacent paracancerous tissues. N'-nitrosonicotinic acid (NNN) is a known carcinogen in tobacco, and its role in the development and progression of HCC remains unclear. CCK-8 assays showed that overexpression of SLC10A1 significantly inhibited the proliferation of HepG2 and HCCLM3 cells. Scratch and Transwell assays showed that overexpression of SLC10A1 significantly reduced cell migration. Furthermore, overexpression of SLC10A1 inhibited the adhesion of both cell lines to various extracellular matrix components, including type I collagen, fibronectin, and polylysine. Compared to the control group, the number of clones formed in the SLC10A1 overexpression group was significantly reduced. In cisplatin treatment experiments, overexpression of SLC10A1 reduced the half-maximal inhibitory concentration (IC50) of cisplatin. Furthermore, NNN-treated hepatocellular carcinoma cells exhibited enhanced proliferative capacity. Western blot analysis showed that SLC10A1 overexpression reduced AKT and ERK phosphorylation levels, effectively inhibiting the PI3K/AKT and MAPK/ERK signaling pathways. Therefore, these results indicate that SLC10A1 has an inhibitory effect on the proliferation, migration, adhesion, and colony formation of hepatocellular carcinoma cells. These inhibitory effects are achieved by inhibiting the PI3K/AKT and MAPK/ERK signaling pathways.
Clonogenic assays showed that SLC10A1-overexpressing HepG2 and HCCLM3 cells formed significantly fewer colonies than control cells (p < 0.001 for HepG2; p < 0.0001 for HCCLM3) (Figure 1A). To explore SLC10A1's role in tumor microenvironment interactions, researchers quantified adhesion to extracellular matrix components (fibronectin, collagen I and poly-L-lysine). The results showed that SLC10A1 overexpression reduced adhesion to all tested substrates in HepG2 (p < 0.01 for fibronectin; p < 0.001 for collagen I; p < 0.0001 for poly-L-lysine) and HCCLM3 cells (p < 0.01 for fibronectin; p < 0.001 for collagen I and poly-L-lysine) (Figure 1B). These results indicate that SLC10A1 extensively disrupts tumor-stroma adhesion mechanisms.
Figure 1. SLC10A1 inhibits HCC cells colony formation and cells adhesion. (Fan W, et al. 2025)
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