Panoply™ Human LIFR Knockdown Stable Cell Line

Name: Panoply™ Human LIFR Knockdown Stable Cell Line
SKU: CSC-DC008696
Availability: InStock

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

Cat. No. : CSC-DC008696

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

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Gene Information

Cat. No.	CSC-DC008696
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	LIFR
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	LIFR leukemia inhibitory factor receptor alpha [ Homo sapiens ]
Gene Symbol	LIFR
Synonyms	SWS; SJS2; STWS; CD118; LIF-R
Gene ID	3977
Uni Prot ID	A8K1Z4
m RNA Refseq	NM_001127671.1
Protein Refseq	NP_001121143.1
Chromosome Location	5p13-p12
Function	contributes_to ciliary neurotrophic factor receptor activity; ciliary neurotrophic factor receptor binding; cytokine binding; growth factor binding; leukemia inhibitory factor receptor activity; contributes_to leukemia inhibitory factor receptor activity; contributes_to oncostatin-M receptor activity;
Pathway	Adipogenesis, organism-specific biosystem; Cytokine-cytokine receptor interaction, organism-specific biosystem; Cytokine-cytokine receptor interaction, conserved biosystem; Jak-STAT signaling pathway, organism-specific biosystem; Jak-STAT signaling pathway, conserved biosystem;
MIM	151443

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Pancreatic cancer (PC) is one of the leading causes of cancer-related mortality worldwide. Frequent metastasis and recurrence are the main reasons for poor prognosis in PC patients. Therefore, the discovery of new biomarkers and a deeper understanding of the mechanisms of pancreatic tumorigenesis and metastasis are crucial. Here, researchers report that leukemia inhibitory factor receptor (LIFR) inhibits PC cell tumorigenesis and metastasis both in vitro and in vivo. LIFR expression is significantly reduced in PC tissues and correlates with local invasion, lymph node metastasis, and tumor node metastasis (TNM) stage. In vitro, LIFR overexpression significantly inhibits PC cell colony formation, migration, invasion, and wound repair, while LIFR silencing exhibits the opposite effect. Furthermore, animal xenograft and metastasis models confirm the in vivo and in vitro results. LIFR also inhibits the expression of β-catenin, vimentin, and slug, while inducing E-cadherin expression, suggesting a possible mechanism of action involving the epithelial-mesenchymal transition pathway and a negative regulatory role for LIFR in PC cell metastasis.

Clinical invasion characteristics of pancreatic cancer patients are closely correlated with LIFR expression levels, suggesting that LIFR may play a negative regulatory role in pancreatic cancer metastasis. To confirm the effect of LIFR on pancreatic cancer cell metastasis, researchers conducted Transwell migration and invasion assays. As shown in Figures 1A and B, LIFR-knockdown Capan-1 cells significantly enhanced their migration and invasion abilities. Conversely, overexpression of LIFR in pancreatic cancer cells significantly reduced the migration and invasion abilities of PATU-8988 cells. Furthermore, the researchers quantitatively investigated the effect of LIFR on cell migration using a wound wound assay. Compared with control cells, the distance between the scratch edges in LIFR-knockdown Capan-1 cells was significantly shortened (Figures 1E and 1G). Consistent with this, overexpression of LIFR in PATU-8988 cells prolonged the wound healing distance (Figures 1F and G). Taken together, these results demonstrate that the invasive and highly metastatic phenotype of PC cells can be regulated in vitro by LIFR.

Figure 1. LIFR negatively regulates the metastasis of PC cells in vitro. (Ma D, et al., 2016)

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