Cat.No. : CSC-SC008501 Host Cell: HEK293 (CHO and other cell types are also available)
| Cat. No. | CSC-SC008501 |
| 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 | L1CAM |
| 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 | L1CAM L1 cell adhesion molecule [ Homo sapiens ] |
| Gene Symbol | L1CAM |
| Synonyms | S10; HSAS; MASA; MIC5; SPG1; CAML1; CD171; HSAS1; N-CAML1; NCAM-L1; N-CAM-L1 |
| Gene ID | 3897 |
| UniProt ID | P32004 |
| mRNA Refseq | NM_000425.3 |
| Protein Refseq | NP_000416.1 |
| Chromosome Location | Xq28 |
| Pathway | Axon guidance, organism-specific biosystem; Axon guidance, conserved biosystem; Axon guidance, organism-specific biosystem; Basigin interactions, organism-specific biosystem; Cell adhesion molecules (CAMs), organism-specific biosystem; Cell adhesion molecules (CAMs), conserved biosystem; Cell surface interactions at the vascular wall, organism-specific biosystem; |
| MIM | 308840 |
| 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 |
L1 cell adhesion molecule (L1CAM) exhibits oncogenic activity in tumors. However, the link between L1CAM and the tumor microenvironment remains unclear in patients with esophageal squamous cell carcinoma (ESCC). Here, researchers investigated how L1CAM expression in ESCC influences the oncogenic properties of tumor cells and the tumor microenvironment. Studies have shown that L1CAM expression is significantly elevated in ESCC tissues and correlates with poor prognosis. Ablation of L1CAM in ESCC cells inhibited tumor growth and migration, and increased tumor cell apoptosis. Within the tumor microenvironment, L1CAM expression is associated with Treg infiltration in ESCC by affecting CCL22 secretion. Mechanistically, L1CAM promotes CCL22 expression by activating the PI3K/Akt/NF-κB signaling pathway. Furthermore, CCL22 promotes Treg recruitment to tumor sites. Tregs subsequently secrete TGF-β, which in turn promotes L1CAM expression through Smad2/3, forming a positive feedback loop. These findings provide new insights into the mechanisms of L1CAM-mediated immune escape and suggest that targeting the L1CAM-CCL22-TGF-β crosstalk between tumor cells and Tregs may provide a unique approach to improve the treatment of patients with esophageal squamous cell carcinoma.
L1CAM primarily regulates immune and chemokine pathways (Figures 1A and 1B). To further identify factors mediating communication between cancer and immune cells in this context, researchers performed cytokine array analysis using a human multiplex bead-based kit and found that CCL22 was significantly downregulated in shL1CAM cells (Figure 1C, upper panel), while it was significantly upregulated at the protein level in L1CAM-overexpressing cells (Figure 1C, lower panel). These results were confirmed by qRT-PCR and ELISA (Figures 1D and 1E). Subsequently, to further confirm these findings, researchers examined CCL22 expression in the subcutaneous tumor samples shown in Figure 1J using qRT-PCR and IHC. CCL22 expression was significantly lower in shL1CAM EC1 cells than in shNC cells, while it was higher in L1CAM-overexpressing KYSE450 cells than in shNC cells (Figures 1F, 1G, and 1H). The expression of CCL22 parallels that of L1CAM. The in vivo results are consistent with the in vitro results. These results suggest that L1CAM may promote the expression of CCL22.
Figure 1. L1CAM promotes the recruitment of Tregs by upregulating CCL22. (Zhao X, et al., 2021)
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