Panoply™ Human SLC34A2 Knockdown Stable Cell Line

Name: Panoply™ Human SLC34A2 Knockdown Stable Cell Line
SKU: CSC-DC014507
Availability: InStock

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

Cat. No. : CSC-DC014507

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

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Gene Information

Cat. No.	CSC-DC014507
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	SLC34A2
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	SLC34A2 solute carrier family 34 (sodium phosphate), member 2 [ Homo sapiens ]
Gene Symbol	SLC34A2
Synonyms	NPTIIb; NAPI-3B; NAPI-IIb
Gene Description	solute carrier family 34 (sodium phosphate), member 2
GeneID	10568
Uni ProtID	O95436
mRNA Refseq	NM_006424.2
Protein Refseq	NP_006415.2
Chromosome Location	4p15.2
Function	phosphate ion binding; sodium ion binding; sodium-dependent phosphate transmembrane transporter activity; sodium:phosphate symporter activity;
Pathway	Mineral absorption, organism-specific biosystem; Mineral absorption, conserved biosystem; SLC-mediated transmembrane transport, organism-specific biosystem; Sodium-coupled phosphate cotransporters, organism-specific biosystem; Transmembrane transport of small molecules, organism-specific biosystem; Transport of inorganic cations/anions and amino acids/oligopeptides, organism-specific biosystem; Type II Na+/Pi cotransporters, organism-specific biosystem;
MIM	604217

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Solute carrier 34 A2 (SLC34A2) is a member of the SLC34 family, a class of phosphate transporters. SLC34A2 has been reported to play a key role in tumorigenesis and progression. However, the biological role of SLC34A2 in gliomas remains unknown. Here, researchers analyzed the expression patterns of SLC34A2 in clinical glioma tissues and cell lines. Results showed that SLC34A2 is universally overexpressed in glioma tissues and cell lines. To further investigate the role of SLC34A2 in glioma, researchers generated SLC34A2 knockdown glioma cell lines U251 and U87. Subsequent studies demonstrated that SLC34A2 knockdown inhibited cell proliferation and migration/invasion. SLC34A2 knockdown also suppressed the epithelial-mesenchymal transition (EMT) phenotype, as demonstrated by increased E-cadherin expression and decreased N-cadherin and fibronectin expression. Furthermore, SLC34A2 knockdown enhanced the sensitivity of U251 and U87 cells to temozolomide (TMZ). In vivo tumorigenesis experiments demonstrated that SLC34A2 knockdown inhibited tumor growth. Furthermore, SLC34A2 knockdown suppressed activation of the epidermal growth factor receptor (EGFR)/PI3K/AKT signaling pathway in U87 cells. The EGFR inhibitor GW2974 enhanced cell proliferation and migration/invasion abilities suppressed by SLC34A2 knockdown and enhanced the sensitivity of glioma cells to TMZ, which was enhanced by SLC34A2 knockdown. These findings suggest that SLC34A2 may be a new potential target for glioma therapy.

To verify the effects of SLC34A2 knockdown on cell migration and invasion, the researchers performed Transwell assays. Compared with control cells, the migration ability of SLC34A2 knockdown U251 and U87 cells was significantly reduced (Figures 1A and B). Consistently, SLC34A2 knockdown also inhibited the invasion ability of U251 and U87 cells (Figures 1C and D). Furthermore, the researchers used Western blot to examine the expression of E-cadherin, N-cadherin, and fibronectin, reflecting the epithelial-mesenchymal transition (EMT) process. In SLC34A2 knockdown U251 and U87 cells, E-cadherin expression was increased, while N-cadherin and fibronectin expression was decreased (Figures 1E and F), indicating that SLC34A2 knockdown can block the EMT process.

Figure 1. Effect of SLC34A2 knockdown on the migration/invasion and EMT process in glioma cells. (Bao Z, et al., 2019)

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