Panoply™ Human PIK3CA Knockdown Stable Cell Line

Name: Panoply™ Human PIK3CA Knockdown Stable Cell Line
SKU: CSC-DC011783
Availability: InStock

For research use only. Not intended for any clinical use.

Cat. No. : CSC-DC011783

Host Cell : HEK293 (Hela and other cell types are also available) Validation : Real-Time RCR

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Gene Information

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.
Target Gene	PIK3CA
Host Cell	HEK293 (Hela and other cell types are also available)
Host Cell Species	Homo sapiens (Human)
Applications	(1) Studying gene functions (2) Studying gene interactions and signaling pathways (3) Target validation and drug discovery (4) Designing diseases models
Size	>1 × 10⁶ cells / vial
Stability	Validated for at least 10 passages
Validation	Real-Time RCR
Quality Control	Negative for bacteria, yeast, fungi and mycoplasma.
Storage	Liquid Nitrogen
Shipping	Dry Ice

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

Gene Name	PIK3CA phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha [ Homo sapiens ]
Gene Symbol	PIK3CA
Synonyms	PI3K; CLOVE; p110-alpha
Gene ID	5290
Uni Prot ID	P42336
m RNA Refseq	NM_006218.2
Protein Refseq	NP_006209.2
Chromosome Location	3q26.3
Function	1-phosphatidylinositol-3-kinase activity; ATP binding; insulin receptor substrate binding; kinase activity; phosphatidylinositol 3-kinase activity; phosphatidylinositol 3-kinase activity; phosphatidylinositol-4,5-bisphosphate 3-kinase activity; protein binding; protein kinase activator activity; protein serine/threonine kinase activity;
Pathway	3-phosphoinositide biosynthesis, organism-specific biosystem; 3-phosphoinositide biosynthesis, conserved biosystem; AMPK signaling, organism-specific biosystem; Acute myeloid leukemia, organism-specific biosystem; Acute myeloid leukemia, conserved biosystem; Adaptive Immune System, organism-specific biosystem; Aldosterone-regulated sodium reabsorption, organism-specific biosystem;
MIM	171834

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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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