Panoply™ Human CXCR1 Knockdown Stable Cell Line

Name: Panoply™ Human CXCR1 Knockdown Stable Cell Line
SKU: CSC-DC003874
Availability: InStock

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

Cat. No. : CSC-DC003874

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

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Gene Information

Cat. No.	CSC-DC003874
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	CXCR1
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	CXCR1 chemokine (C-X-C motif) receptor 1 [ Homo sapiens ]
Gene Symbol	IL8RA
Synonyms	C-C; CD128; CD181; CKR-1; IL8R1; IL8RA; CMKAR1; IL8RBA; CDw128a; C-C-CKR-1
Gene Description	interleukin 8 receptor, alpha
Gene ID	3579
Uni Prot ID	P25024
m RNA Refseq	NM_000634.2
Protein Refseq	NP_000625.1
Chromosome Location	2q35
Function	G-protein coupled receptor activity; chemokine receptor activity; interleukin-8 binding; interleukin-8 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; Endocytosis, organism-specific biosystem;
MIM	146929

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The loss of appropriate cell adhesion normally induces apoptosis via a process termed anoikis. Here, researchers investigated the effects of mesenchymal stem cells (MSCs) within the cancer microenvironment on osteosarcoma (OS) cell resistance to apoptosis and lung metastasis, and evaluated the critical role of the interleukin (IL)-8/C-X-C chemokine receptor (CXCR) 1/Akt signaling pathway in these processes. Metastatic OS subtype cells were isolated from the lung and treated with or without MSC-conditioned medium (MSC-CM) in vitro and designated Saos2-lung-M. Treatment with both MSC-CM and IL-8 enhanced the apoptosis resistance of Saos2 cells in vitro. Furthermore, exogenous MSC-CM promoted the survival and metastasis of Saos2 cells in nude mice. Saos2-lung-M cells were more malignant than their parental cells and were more susceptible to apoptosis. MSC secretion of IL-8 protects OS cells from apoptosis. Blocking the IL-8/CXCR1/Akt pathway by knocking down CXCR1 inhibited lung metastasis of Saos2-lung MSCs and prolonged the survival of tumor-bearing mice. In summary, MSCs enhance the resistance of OS cells to apoptosis and lung metastasis by regulating the IL-8/CXCR1/Akt pathway. These findings suggest that MSCs can "select" OS cells with high metastatic potential in vivo and highlight CXCR1 as a key target in regulating OS cell lung metastasis.

Here, researchers analyzed the in vivo survival of CXCR1-knockdown Saos2-lung-M cells and control Saos2-lung-M cells and found that the survival time of CXCR1-knockdown cells was shorter than that of control cells (Figure 1a, b). Metastatic tumor tissues were collected 4 weeks after injection of CXCR1-knockdown and control Saos2-lung-M cells and immunostained for CXCR1 and p-Akt. HE staining showed that metastatic lymph nodes were smaller, and immunostaining showed that CXCR1 and p-Akt expression was reduced in CXCR1-knockdown mice compared with control mice (Figure 1c, d). These data indicate that CXCR1 knockdown significantly reduced tumor size and metastasis rate and reduced CXCR1/Akt expression (Figure 1e).

Figure 1. Effect of CXCR1 knockdown on OS cell survival in vivo and immunohistochemistry of CXCR1 and p-Akt. (Du L, et al., 2018)

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