Cat.No. : CSC-SC014335 Host Cell: HEK293 (CHO and other cell types are also available)
| Cat. No. | CSC-SC014335 |
| 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 | SLC16A1 |
| 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 | SLC16A1 solute carrier family 16, member 1 (monocarboxylic acid transporter 1) [ Homo sapiens ] |
| Gene Symbol | SLC16A1 |
| Synonyms | MCT; HHF7; MCT1 |
| Gene Description | solute carrier family 16, member 1 (monocarboxylic acid transporter 1) |
| Gene ID | 6566 |
| UniProt ID | P53985 |
| mRNA Refseq | NM_003051.3 |
| Protein Refseq | NP_003042.3 |
| Chromosome Location | 1p12 |
| Function | mevalonate transmembrane transporter activity; monocarboxylic acid transmembrane transporter activity; secondary active monocarboxylate transmembrane transporter activity; symporter activity; |
| Pathway | Basigin interactions, organism-specific biosystem; Cell surface interactions at the vascular wall, organism-specific biosystem; Hemostasis, organism-specific biosystem; Metabolism, organism-specific biosystem; Proton-coupled monocarboxylate transport, organism-specific biosystem; Pyruvate metabolism, organism-specific biosystem; Pyruvate metabolism and Citric Acid (TCA) cycle, organism-specific biosystem; |
| MIM | 600682 |
| 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 solute carrier family 16, member 1 (SLC16A1) gene is aberrantly expressed in a variety of human malignancies and plays a key role in tumor development and progression. However, the specific mechanisms of action of this gene in head and neck squamous cell carcinoma (HNSCC) remain to be elucidated. Here, researchers combined bioinformatics analysis with clinical patient samples to reveal that SLC16A1 mRNA and protein levels are significantly upregulated in HNSCC patients and are closely associated with poor patient prognosis. Furthermore, by establishing stable SLC16A1 knockdown and overexpression models in HNSCC cells and combining in vitro and in vivo experiments, they comprehensively elucidated the key role of SLC16A1 in promoting HNSCC cell proliferation, migration, and invasion, as well as enhancing its resistance to ferroptosis. In vitro results demonstrated that knockdown of SLC16A1 significantly reduced the proliferation, migration, and invasion abilities of HNSCC cell lines, and increased RAS selective lethal factor 3-induced lipid peroxidation compared with control cells. Conversely, SLC16A1-overexpressing HNSCC cell lines exhibited enhanced proliferation, migration, and invasion, while also exhibiting reduced lipid peroxidation. In vivo experiments further confirmed the critical role of SLC16A1 in promoting HNSCC tumor growth. These findings suggest that SLC16A1 functions as an oncogene in HNSCC, and that abnormally high expression of SLC16A1 significantly accelerates the development and progression of HNSCC by conferring resistance to ferroptosis.
Given that migration and invasion are key features of tumorigenesis and progression, the researchers conducted in vitro migration and invasion assays using HNSCC cell lines with varying levels of SLC16A1 expression. They initially performed wound healing and Transwell assays using SLC16A1 knockdown TU177 cells and their corresponding control cells. Notably, SLC16A1 knockdown significantly reduced the migration and invasion abilities of TU177 cells compared to control cells (Figure 1A-B). Conversely, in SLC16A1-overexpressing HN6 cells, their migration and invasion abilities were significantly enhanced compared to control cells (Figure 1C-D).
Figure 1. SLC16A1 promotes HNSCC cell migration and invasion. (Zong H, et al., 2025)
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