Cat.No. : CSC-SC009930 Host Cell: HEK293 (CHO and other cell types are also available)
| Cat. No. | CSC-SC009930 |
| 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 | MUC16 |
| 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. |
| 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 |
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancer types, frequently metastasizing to the liver and resulting in a poor overall prognosis. Previous studies have shown that MUC16 and its C-terminal (Cter) domain are associated with the aggressive nature of PDAC. Here, researchers observed significantly elevated expression of MUC16 and its Cter in human PDAC tissue, PDAC organoids, and metastatic liver tissue using immunohistochemistry (IHC) and immunofluorescence (IFC) analysis, whereas expression was absent in normal pancreatic tissue. Knockdown of MUC16 in SW1990 and CD18/HPAF PDAC cells significantly reduced colony formation, migration, and endothelial cell/P-selectin binding. Conversely, ectopic overexpression of MUC16-Cter significantly enhanced clonogenicity and migration in MiaPaCa2 pancreatic cancer cells. Notably, MUC16 promoted cell survival and colonization in the liver, mimicking an in vitro environment. Furthermore, MUC16 enhanced liver metastasis in an in vivo mouse model. Integrated RNA sequencing analysis revealed that MUC16 alters neuropilin-2 (NRP2) and cell adhesion molecules in pancreatic cancer cells. Furthermore, the researchers discovered that MUC16 regulates NRP2 in pancreatic cancer cells through the JAK2/STAT1 signaling pathway. In pancreatic cancer cells overexpressing MUC16, knockdown of NRP2 significantly reduced cell adhesion and migration. Together, these findings suggest that MUC16 regulates NRP2 and induces pancreatic cancer cell metastasis.
Validation of cell adhesion genes revealed significant differences in gene expression of cadherin 24, desmocollin 3, and protocadherin B12 between knockout/knockdown and overexpression models (Figure 1A). Furthermore, desmocollin 3 and protocadherin B12 expression levels were decreased in pancreatic cancer cells harboring Capan1 MUC16 knockout, but increased in MiaPaCa2 cells overexpressing MUC16-Cter (Figure 1B and C). These results strongly suggest that MUC16 plays a critical role in regulating cell adhesion-promoting genes in pancreatic cancer (PDAC). qRT-PCR data revealed that mRNA expression of PTHLH, IGFBP2, GADD45A, FBLN2, PTTG1, JUN, SERPINE1, TGFBI, and NRP2 was commonly altered in both MUC16 knockout and MUC16-Cter-overexpressing pancreatic cancer cells (Figure 1D). Absolute quantification by ddPCR revealed that the copy numbers of SERPINE1, NRP2, IGFBP2, and PTTG1 genes were significantly decreased in MUC16 knockout cells but significantly increased in MUC16-Cter-overexpressing pancreatic cancer cells. Notably, the researchers identified MUC16-mediated metastatic genes, such as PAI1 (SERPINE1), IGFBP2, and NRP2, in pancreatic cancer cells. Immunoblotting and immunofluorescence analysis demonstrated that NRP2 expression was decreased in MUC16 knockout/knockdown Capan1/SW1990 cells, while NRP2 was overexpressed in MUC16-Cter-overexpressing T3M4 and MiaPaCa2 cells (Figures 1E and F).
Figure 1. MUC16 regulation of cell adhesion-promoting molecules and metastatic gene NRP2 regulation through activation of JAK2/STAT1 axis. (Marimuthu S, et al., 2022)
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