Cat.No. : CSC-DC011550
Host Cell: HEK293 (Hela and other cell types are also available) Validation: Real-Time RCR
| Cat. No. | CSC-DC011550 |
| Description | Creative Biogene's Knockdown Cell Lines are target specific shRNA lentivirus transduced cells. The percent knockdown levels range from 75-99% depending on the gene, as evaluated by Real-Time RCR. Cells are rigorously qualified and mycoplasma free. |
| Gene | PDPK1 |
| Host Cell | HEK293 (Hela and other cell types are also available) |
| Host Cell Species | Homo sapiens (Human) |
| Stability | Validated for at least 10 passages |
| Application | (1) Studying gene functions (2) Studying gene interactions and signaling pathways (3) Target validation and drug discovery (4) Designing diseases models |
| Quality Control | Negative for bacteria, yeast, fungi and mycoplasma. |
| Size Form | >1 × 10^6 cells / vial |
| Shipping | Dry Ice |
| Storage | Liquid Nitrogen |
| Gene Name | Pdpk1 3-phosphoinositide dependent protein kinase 1 [ Mus musculus ] |
| Gene Symbol | Pdpk1 |
| Synonyms | Pdk1 |
| Gene Description | 3-phosphoinositide dependent protein kinase-1 |
| Gene ID | 18607 |
| UniProt ID | Q3TRL2 |
| mRNA Refseq | NM_001080773.1 |
| Protein Refseq | NP_001074242.1 |
| Chromosome Location | 17 A3.3; 17 |
| Function | 3-phosphoinositide-dependent protein kinase activity; 3-phosphoinositide-dependent protein kinase activity; ATP binding; insulin receptor binding; kinase activity; nucleotide binding; protein kinase activity; protein kinase binding; protein serine/threonine kinase activity; transferase activity; transferase activity, transferring phosphorus-containing groups; |
| Pathway | Activation of NMDA receptor upon glutamate binding and postsynaptic events, organism-specific biosystem; Activation of PKB, organism-specific biosystem; Adaptive Immune System, organism-specific biosystem; Aldosterone-regulated sodium reabsorption, organism-specific biosystem; Aldosterone-regulated sodium reabsorption, conserved biosystem; B Cell Receptor Signaling Pathway, organism-specific biosystem; CD28 co-stimulation, organism-specific biosystem; |
| 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 |
Epithelial ovarian cancer (EOC) is a common estrogen-sensitive tumor that seriously threatens women's health, and its mortality rate ranks first among female malignant tumors. Studies have shown that estrogen abnormalities are closely related to the progression of EOC. 3-phosphoinositide-dependent protein kinase-1 (PDPK1) is highly expressed in EOC tissues. Furthermore, estrogen can upregulate the expression of PDPK1 in EOC cells. Here, researchers found that high expression of PDPK1 is associated with poor prognosis in ovarian cancer patients. In addition, estrogen stimulates the increased expression of PDPK1 protein through the estrogen receptor ESR1. The absence or overexpression of PDPK1 affects the inhibition or enhancement of estrogen-driven EOC cell proliferation, while knockdown of PDPK1 can inhibit estrogen-induced EOC cell migration and promote apoptosis. This indicates an important functional link between estrogen and PDPK1 in the development and progression of EOC. Under estrogen treatment, PDPK1 can regulate the messenger RNA expression of cyclin A1, cyclin-dependent kinase 2 (CDK2), matrix metalloproteinase 2 (MMP2), and Bcl-2-associated X protein (Bax). These findings suggest that PDPK1 plays an oncogenic role in the development and progression of EOC.
To elucidate the role of PDPK1 in E2-induced SK-OV-3 cells, researchers examined the physiological functions of PDPK1-knockdown SK-OV-3 cells under E2 stimulation, including changes in cell proliferation, migration, and apoptosis levels. The researchers used EdU staining to detect the effect of PDPK1 on the proliferation of E2-stimulated SK-OV-3 cells. The results showed that E2 significantly promoted the proliferation of SK-OV-3 cells (Figure 1B and b). In contrast, in PDPK1-knockdown SK-OV-3 cells, the proliferative effect of E2 was inhibited. Subsequently, cell migration experiments showed that E2 significantly promoted the migration of SK-OV-3 cells; however, in PDPK1-knockdown cells, the migration-promoting effect of E2 was inhibited (Figure 1C and c). Since the above results indicated that the absence of PDPK1 inhibited E2-induced SK-OV-3 cell proliferation and migration, the researchers used flow cytometry to detect the potential role of E2 and PDPK1 in altering SK-OV-3 cell apoptosis. They found that E2 induced late apoptosis (Figure 1D and d), while interfering with PDPK1 exacerbated late apoptosis and cell death. In summary, these results indicate that E2 exhibits significant pro-cancer effects in SK-OV-3 cells in a PDPK1-dependent manner.
Figure 1. Knock-down of PDPK1 suppresses E2-driven SK-OV-3 cells proliferation and migration but promotes apoptosis. (Wang Y, et al., 2024)
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