Panoply™ Human CCR3 Knockdown Stable Cell Line

Name: Panoply™ Human CCR3 Knockdown Stable Cell Line
SKU: CSC-DC002673
Availability: InStock

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

Cat. No. : CSC-DC002673

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

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Gene Information

Cat. No.	CSC-DC002673
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	CCR3
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	CCR3 chemokine (C-C motif) receptor 3 [ Homo sapiens ]
Gene Symbol	CCR3
Synonyms	CKR3; CD193; CMKBR3; CC-CKR-3
GeneID	1232
Uni ProtID	Q8TDP4
mRNA Refseq	NM_001164680.1
Protein Refseq	NP_001158152.1
Chromosome Location	3p21.3
Function	C-C chemokine receptor activity; chemokine receptor activity;
Pathway	Chemokine receptors bind chemokines, organism-specific biosystem; Chemokine signaling pathway, organism-specific biosystem; Chemokine signaling pathway, conserved biosystem; Class A/1 (Rhodopsin-like receptors), organism-specific biosystem; Cytokine-cytokine receptor interaction, organism-specific biosystem; Cytokine-cytokine receptor interaction, conserved biosystem; G alpha (i) signalling events, organism-specific biosystem;
MIM	601268

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Myeloid-derived suppressor cells (MDSCs) inhibit anti-tumor immunity and promote cancer progression. While the concept of immunosuppressive MDSCs is well established, the mechanisms by which they regulate non-small cell lung cancer (NSCLC) progression through paracrine signaling remain unclear. Here, researchers found that MDSC infiltration in NSCLC tissues correlates with cancer progression and is positively associated with the development of patient-derived xenograft models and poor patient prognosis. Intratumoral MDSCs directly promote NSCLC metastasis and overexpress chemokines, including CCL11, that promote NSCLC cell invasion. CCL11 activates the AKT and ERK signaling pathways, promoting NSCLC metastasis through the epithelial-mesenchymal transition (EMT) process. Furthermore, elevated CCL11 expression is associated with poor prognosis in lung cancer and other cancer types. These findings emphasize that MDSCs produce CCL11, which promotes NSCLC metastasis by activating ERK and AKT signaling and inducing EMT, suggesting that the MDSCs-CCL11-ERK/AKT-EMT axis comprises a potential target for the treatment of NSCLC metastasis.

Since CCR3 has been identified as the primary receptor for CCL11 in cancer cells, researchers sought to assess the importance of the CCL11-CCR3 interaction in non-small cell lung cancer (NSCLC) metastasis. Here, they performed gene expression analysis of CCR3 knockdown in A549 cells as well as A549 cells treated with CCL11 using RNA-Seq. The PI3K-AKT and Ras-MAPK-ERK pathways were identified as significantly important pathways in CCL11-treated cells (Figure 1A, C) and CCR3 knockdown cells (Figure 1B, C), respectively. Furthermore, researchers demonstrated elevated phosphorylation of ERK1/2 and AKT in invasive tumors (Figure 1D). ERK and AKT are key switches in upstream signaling that promote cell migration. Together, these results suggest that ERK and AKT signaling are crucial in CCL11-induced NSCLC cell metastasis.

Figure 1. AKT and ERK signaling pathways may be involved in CCL11-mediated NSCLC metastasis. (Lin S, et al., 2021)

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