Panoply™ Human RRM2 Knockdown Stable Cell Line

Name: Panoply™ Human RRM2 Knockdown Stable Cell Line
SKU: CSC-DC013627
Availability: InStock

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

Cat. No. : CSC-DC013627

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

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Gene Information

Cat. No.	CSC-DC013627
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	RRM2
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	RRM2 ribonucleotide reductase M2 [ Homo sapiens ]
Gene Symbol	RRM2
Synonyms	RRM2; ribonucleotide reductase M2; ribonucleotide reductase M2 polypeptide; ribonucleoside-diphosphate reductase subunit M2; ribonucleotide reductase small chain; ribonucleotide reductase small subunit; R2; RR2; RR2M;
GeneID	6241
Uni ProtID	P31350
mRNA Refseq	BC001886
Chromosome Location	2p25-p24
Function	oxidoreductase activity; ribonucleoside-diphosphate reductase activity; ribonucleoside-diphosphate reductase activity; transition metal ion binding;
Pathway	Cell Cycle, organism-specific biosystem; Cell Cycle, Mitotic, organism-specific biosystem; E2F mediated regulation of DNA replication, organism-specific biosystem; E2F transcription factor network, organism-specific biosystem; Fluoropyrimidine Activity, organism-specific biosystem; G1/S Transition, organism-specific biosystem; G1/S-Specific Transcription, organism-specific biosystem;
MIM	180390

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Glioma is one of the most common brain tumors, making the study of its molecular mechanisms crucial. Here, researchers investigated the role of ribonucleotide reductase regulatory subunit M2 (RRM2) in glioma. TCGA data, Western blot, and immunohistochemistry results all showed that RRM2 expression levels were higher in glioma tissues. RRM2 expression levels were negatively correlated with the survival rate of glioma patients. RNA sequencing results showed that after RNAi-mediated RRM2 gene knockdown, the expression of genes involved in apoptosis, proliferation, cell adhesion, and negative regulation of signal transduction was upregulated. In an in vivo model, RRM2 knockdown inhibited tumor growth and suppressed the AKT and ERK1/2 signaling pathways. Interfering with RRM2 also downregulated the expression of cyclin A, cyclin B1, cyclin D1, vimentin, and N-cadherin, and upregulated the expression of E-cadherin. Furthermore, when AKT and ERK1/2 phosphorylation were inhibited by LY294002 or PD98059, RRM2 overexpression failed to increase the expression of cyclin B1, cyclin D1, and N-cadherin. These findings suggest that RRM2 is a positive regulator of glioma progression, promoting glioma cell migration and proliferation through the ERK1/2 and AKT signaling pathways, and may serve as a novel prognostic indicator for glioma patients.

To investigate the effect of RRM2 on the migration of U87 and LN-229 cells, researchers employed wound healing and Transwell migration assays. Representative micrographs were taken every 12 hours after creating a scratch in the cell monolayer. Compared to the control group, the migration ability of RRM2-knockdown U87 and LN-229 cells was significantly reduced. Furthermore, Transwell migration assay results also showed that silencing RRM2 expression in U87 and LN-229 cells decreased the number of migrating cells (Figure 1A-D). To further explore the potential role of RRM2 in glioma cell migration, researchers investigated the role of RRM2 in regulating EMT biomarkers. The results showed that in RRM2-knockdown cells, E-cadherin levels were upregulated, while N-cadherin and vimentin levels were downregulated (Figure 1E-F). Therefore, RRM2 overexpression may promote glioma cell migration.

Figure 1. Knockdown of RRM2 inhibits the migration of glioma cells. (Sun H, et al., 2019)

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