Panoply™ Human PDE4B Knockdown Stable Cell Line

Name: Panoply™ Human PDE4B Knockdown Stable Cell Line
SKU: CSC-DC011504
Availability: InStock

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

Cat. No. : CSC-DC011504

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

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Cell Line Information

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Gene Information

Cat. No.	CSC-DC011504
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	PDE4B
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	PDE4B phosphodiesterase 4B, cAMP-specific [ Homo sapiens ]
Gene Symbol	PDE4B
Synonyms	DPDE4; PDE4B5; PDEIVB
Gene Description	phosphodiesterase 4B, cAMP-specific (phosphodiesterase E4 dunce homolog, Drosophila)
GeneID	5142
Uni ProtID	Q07343
mRNA Refseq	NM_001037340.1
Protein Refseq	NP_001032417.1
Chromosome Location	1p31
Function	3,5-cyclic-AMP phosphodiesterase activity; metal ion binding;
Pathway	DARPP-32 events, organism-specific biosystem; G Protein Signaling Pathways, organism-specific biosystem; G alpha (s) signalling events, organism-specific biosystem; GPCR downstream signaling, organism-specific biosystem; Integrated Pancreatic Cancer Pathway, organism-specific biosystem; Morphine addiction, organism-specific biosystem; Morphine addiction, conserved biosystem;
MIM	600127

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Phosphodiesterase 4B (PDE4B) is a key enzyme regulating intracellular cyclic adenosine monophosphate (cAMP) levels, playing a crucial role in the diagnosis, classification, treatment, and prognosis of various cancers. However, the role of PDE4B in gastric cancer (GC) remains unclear. Here, researchers demonstrate that PDE4B is highly expressed in GC and is significantly correlated with tumor invasion depth, distant metastasis, TNM stage, and preoperative CA199 levels. PDE4B overexpression promotes the proliferation, colony formation, migration, and invasion of GC cancer cells and is associated with poor prognosis. PDE4B promotes the infiltration of immune cells into the tumor microenvironment (TME) and activates the PI3K/AKT pathway, thereby increasing MYC expression. PDE4B can serve as an independent prognostic biomarker for GC. Researchers found that PDE4B can promote immune cell infiltration into the TME through the PI3K/AKT/MYC pathway and mediate the malignant progression of GC.

To investigate the role of PDE4B in the development and progression of gastric cancer, researchers constructed a PDE4B knockdown HGC-27 gastric cancer cell line. Since PDE4B is known to hydrolyze the second messenger cAMP, they used Western blot (WB) to detect changes in cAMP levels (Figures 1A and 1B). Cell proliferation (CCK-8) assays showed that the proliferation of PDE4B knockdown gastric cancer cells was inhibited (Figure 1C). Subsequent clonogenic assays further confirmed the adverse effect of PDE4B knockdown on cell viability (Figure 1D). Transwell assays also showed that the invasion and migration of PDE4B knockdown gastric cancer cells were inhibited (Figures 1E and 1F). Flow cytometry analysis showed increased apoptosis after PDE4B knockdown (Figure 1G). Finally, the researchers constructed a tumor xenograft model to determine the role of PDE4B in the development and progression of gastric cancer in vivo. The results showed that, compared with the control group, the volume and weight of subcutaneous tumors in the PDE4B knockdown group were significantly reduced (Figures 1H-J). These results indicate that PDE4B knockdown inhibits the malignant biological characteristics of gastric cancer.

Figure 1. PDE4B plays an oncogenic role in GC cells. (Su R, et al., 2024)

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