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Panoply™ Human GREM1 Knockdown Stable Cell Line

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

Cat. No. :   CSC-DC006640

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

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Gene Information

Cat. No. CSC-DC006640
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 GREM1
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 GREM1 gremlin 1 [ Homo sapiens ]
Gene Symbol GREM1
Synonyms GREM1; gremlin 1; CKTSF1B1, cysteine knot superfamily 1, BMP antagonist 1 , gremlin 1, cysteine knot superfamily, homolog (Xenopus laevis); gremlin-1; DAND2; DRM; gremlin; gremlin 1-like protein; DAN domain family member 2; increased in high glucose-2; proliferation-inducing gene 2; increased in high glucose protein 2; cell proliferation-inducing gene 2 protein; cysteine knot superfamily 1, BMP antagonist 1; gremlin 1, cysteine knot superfamily, homolog; down-regulated in Mos-transformed cells protein; PIG2; IHG-2; GREMLIN; CKTSF1B1; MGC126660;
GeneID 2908
Uni ProtID O60565
mRNA Refseq BC069525
Chromosome Location 15q13.3
Function cytokine activity; protein binding;
Pathway BMP receptor signaling, organism-specific biosystem;
MIM 603054
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Gremlin-1 (GREM1) is a bone morphogenetic protein (BMP) antagonist capable of directly binding to BMPs. GREM1 is involved in processes such as organogenesis, tissue differentiation, and organ fibrosis. Numerous studies have reported the pro-tumorigenic role of GREM1 in cancer. In this study, researchers evaluated the role of GREM1 in breast cancer progression by assessing the growth, migration, and invasion capabilities of breast cancer cells; they also investigated the effect of GREM1 on lung metastasis using an orthotopic mouse model of breast cancer. The results demonstrated that GREM1 knockdown inhibited breast cancer cell proliferation, whereas GREM1 overexpression promoted cell growth, migration, and invasion. Compared with the control group, the GREM1 knockdown group exhibited significantly reduced tumor growth rates and a marked decrease in the incidence of lung metastasis. GREM1 was found to upregulate the expression of matrix metalloproteinase 13 (MMP13), and a positive correlation between GREM1 and MMP13 expression was observed in breast cancer patient samples. Mechanistic studies revealed that GREM1 activates Signal Transducer and Activator of Transcription 3 (STAT3), a transcription factor involved in regulating MMP13 expression. These findings suggest that GREM1 may promote lung metastasis in breast cancer cells via the STAT3-MMP13 signaling pathway. Furthermore, GREM1 represents a promising therapeutic target for treating breast cancer metastasis.

To elucidate the role of GREM1 in the growth and migration of breast cancer cells, researchers generated GREM1-knockdown breast cancer cell lines (MDA-MB-231 and MTV/TM-011) (Figure 1A). Subsequently, they assessed the effect of GREM1 on cell growth using these cell lines and found that GREM1 knockdown inhibited cell proliferation (Figure 1B). To investigate the impact of GREM1 on the migratory capacity of breast cancer cells, the researchers performed wound-healing assays. The results demonstrated that the migration rate of GREM1-knockdown cells was significantly slower compared to that of control cells (Figure 1C–F).

Figure 1. GREM1 knockdown inhibits the growth and mobility of breast cancer cells.Figure 1. GREM1 knockdown inhibits the growth and mobility of breast cancer cells. (Sung N J, et al., 2020)

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