Cat.No. : CSC-DC011783
Host Cell: HEK293 (Hela and other cell types are also available) Validation: Real-Time RCR
| Cat. No. | CSC-DC011783 |
| 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 | PIK3CA |
| 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 | PIK3CA phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha [ Gallus gallus (chicken) ] |
| Gene Symbol | PIK3CA |
| Synonyms | PIK3CA; phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha; C-P3K; phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha isoform; phosphoinositide 3-kinase catalytic subunit; phosphoinositide-3-kinase, catalytic, alpha polypeptide; |
| Gene Description | phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha |
| Gene ID | 424971 |
| UniProt ID | O42391 |
| mRNA Refseq | NM_001004410 |
| Protein Refseq | NP_001004410 |
| Chromosome Location | chromosome: 9 |
| Pathway | Adrenergic signaling in cardiomyocytes; Apoptosis; EGFR1 Signaling Pathway; ErbB signaling pathway; Focal adhesion; FoxO signaling pathway; G13 Signaling Pathway; |
| 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 |
PIK3CA is a key component of the phosphatidylinositol 3-kinase (PI3K) pathway, and previous studies have confirmed its involvement in tumorigenesis. However, its function and underlying mechanisms in bladder cancer remain largely unclear. Here, researchers used tissue microarray (TMA) technology to perform immunohistochemical staining on tissue samples from 66 bladder cancer patients to detect the expression levels of PIK3CA and CUX1. The results showed that PIK3CA was upregulated in bladder cancer tissues, and patients with high PIK3CA expression had a poorer prognosis. PIK3CA overexpression promoted the growth, migration, invasion, and metastasis of bladder cancer cells, while PIK3CA knockdown had the opposite effect. Gain-of-function and loss-of-function studies demonstrated that CUX1 promotes PIK3CA expression, thereby activating epithelial-mesenchymal transition (EMT), accompanied by the upregulation of Snail, β-catenin, and Vimentin expression and the downregulation of E-cadherin expression in bladder cancer cell lines. Furthermore, CUX1 overexpression could restore the expression levels of Snail, β-catenin, Vimentin, and E-cadherin caused by PIK3CA knockdown. These results indicate that PIK3CA overexpression in bladder cancer is regulated by the transcription factor CUX1, and that PIK3CA exerts its biological function by activating EMT.
In CCK8 and colony formation assays, cell viability and growth were increased in PIK3CA-overexpressing EJ and T24T cells compared to the control group, while cell viability and growth were decreased in PIK3CA-knockdown cells (Figure 1A). In wound healing assays, PIK3CA overexpression promoted the migration of EJ and T24T cells, while PIK3CA knockdown had the opposite effect (Figure 1B). Transwell assays showed that the invasive ability of PIK3CA-overexpressing cells was enhanced, whereas that of PIK3CA-knockdown cells was reduced (Figure 1C). Furthermore, angiogenesis assays also showed similar effects of PIK3CA on angiogenesis in EJ and T24T cells (Figure 1D).
Figure 1. PIK3CA promoted the growth, migration, invasion and angiogenesis of bladder cancer cells in vitro. (Wang Z, et al., 2020)
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