Panoply™ Human EPHA3 Over-expressing Stable Cell Line

Name: Panoply™ Human EPHA3 Over-expressing Stable Cell Line
SKU: CSC-SC004986
Availability: InStock

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

Cat. No. : CSC-SC004986

Host Cell : HEK293 (CHO and other cell types are also available) Size : >1x10⁶ frozen cells/vial

Inquire for Price

Cell Line Information

Cell Culture Information

Safety and Packaging

Gene Information

Cat. No.	CSC-SC004986
Description	Using Creative Biogene's proprietary lentiviral vectors, we subclone the target gene into lentivector, generate the lentivirus particles, sequentially infect the cell line HEK293 (other cell types are also available according to your requirements), and select the clones constantly expressing target gene at high level.
Target Gene	EPHA3
Gene Species	Homo sapiens (Human)
Host Cell	HEK293 (CHO and other cell types are also available)
Host Cell Species	Species varies
Applications	1. Gene expression studies 2. Signaling pathway research 3. Drug screening and toxicology 4. Disease research
Size	2 × 10^6 cells / vial
Stability	Validated for at least 10 passages
Quality Control	Negative for bacteria, yeast, fungi and mycoplasma.
Storage	Liquid nitrogen
Shipping	Dry Ice

Revival

Rapidly thaw cells in a 37°C water bath. Transfer contents into a tube containing pre-warmed media. Centrifuge cells and seed into a 25 cm2 flask containing pre-warmed media.

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	EPHA3 EPH receptor A3 [ Homo sapiens ]
Gene Symbol	EPHA3
Synonyms	EK4; ETK; HEK; ETK1; HEK4; TYRO4
Gene Description	EPH receptor A3
Gene ID	2042
Uni Prot ID	P29320
m RNA Refseq	NM_005233.5
Protein Refseq	NP_005224.2
Chromosome Location	3p11.2
Function	ATP binding; GPI-linked ephrin receptor activity; protein binding;
Pathway	Axon guidance, organism-specific biosystem; Axon guidance, conserved biosystem; EPHA forward signaling, organism-specific biosystem; EphrinA-EPHA pathway, organism-specific biosystem;
MIM	179611

Quick Inquiry

Case Study

Q & A

Customer Reviews

Eph receptor tyrosine kinases are crucial for intercellular communication during normal and tumorigenesis and development. Eph receptor A3 (EphA3) expression is associated with tumor promotion in some cancer types; however, it plays a tumor-suppressive role in others. Here, researchers used reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Transwell invasion assays to investigate the expression level of EphA3 in esophageal squamous cell carcinoma (ESCC) cell lines and its impact on tumor progression. The results showed that EphA3 expression was decreased in both ESCC tissues and cell lines. Treatment with the DNA methylation inhibitor 5-aza-2'-deoxycytidine increased the mRNA expression level of EphA3 in the ESCC cell lines KYSE510 and KYSE30. Overexpression of EphA3 in KYSE450 and KYSE510 cells inhibited cell migration and invasion. EphA3 overexpression also reduced RhoA GTPase activity. Furthermore, EphA3 overexpression induces epithelial-mesenchymal transition (EMT), manifested as epithelioid morphological changes, increased expression of epithelial proteins (E-cadherin and tight junction protein 1 zonula occludens-1), and decreased expression of mesenchymal proteins (violin, N-cadherin, and Snail). Conversely, silencing EphA3 in KYSE410 cells triggers EMT and promotes cell migration and invasion. These results suggest that EphA3 may play a tumor-suppressive role in esophageal squamous cell carcinoma.

To determine the impact of EphA3 on EMT and MET, researchers analyzed EphA3-overexpressing cells (Figure 1). Notably, characteristic morphological changes associated with MET were observed in stable EphA3-overexpressing KYSE450 and KYSE510 esophageal squamous cell carcinoma (ESCC) cells. As shown in Figure 1A and D, control cells exhibited an elongated shape, characteristic of stromal cells, while EphA3-overexpressing cells displayed the characteristic round shape of epithelial cells. Morphological observation and Transwell assays suggest that EphA3 overexpression may affect the EMT process in ESCC during tumor metastasis. Furthermore, the expression levels of EMT-related genes were detected by RT-qPCR. Compared to control cells, the mRNA expression levels of epithelial cell markers E-cadherin and ZO-1 were upregulated, while the mRNA expression levels of stromal cell markers vimentin and N-cadherin were downregulated (Figures 1B and E). Additionally, the mRNA expression level of Snail, an E-cadherin repressor gene, was also downregulated (Figures 1B and E). Consistent with this, Western blotting results confirmed upregulation of E-cadherin and ZO-1 expression, while downregulation of vimentin expression was observed compared to the vector control cells (Figures 1C and F). These data suggest that EphA3 overexpression may induce mesenchymal-epithelial transition (MET) in KYSE450 and KYSE510 cells.

Figure 1. EphA3 overexpression induces the MET process in KYSE450 and KYSE510 cells. (Chen X, et al., 2019)

Ask a Question

If your question is not addressed through these resources, you can fill out the online form below and we will answer your question as soon as possible.

Question *

Name

Country *

Email *

Write a Review

Write a review of your use of Biogene products and services in your research. Your review can help your fellow researchers make informed purchasing decisions.

Product Name *

Catalog Name *

Rating

Needs improvement

Satisfaction

General satisfaction

Very satisfaction

Product Review Title *

Summary *