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Ephrin Type-B Receptor 6 (EphB6) ELISA Kit
A Biomarker for Non-Small Cell Lung Carcinoma

Alternative name:

  • EphB6
  • Tyrosine-protein kinase-defective receptor EPH-6
  • HEP


Mutations of the EPHB6 receptor tyrosine kinase induce a pro-metastatic phenotype in non-small cell lung cancer

Alterations of Eph receptor tyrosine kinases are frequent events in human cancers. Genetic variations of EPHB6 have been described but the functional outcome of these alterations is unknown. The current study was conducted to screen for the occurrence and to identify functional consequences of EPHB6 mutations in non-small cell lung cancer. Here, we sequenced the entire coding region of EPHB6 in 80 non-small cell lung cancer patients and 3 tumor cell lines. Three potentially relevant mutations were identified in primary patient samples of NSCLC patients (3.8%). Two point mutations led to instable proteins. An in frame deletion mutation (del915-917) showed enhanced migration and accelerated wound healing in vitro. Furthermore, the del915-917 mutation increased the metastatic capability of NSCLC cells in an in vivo mouse model. Our results suggest thatEPHB6 mutations promote metastasis in a subset of patients with non-small cell lung cancer.
Bulk E, et al. PLoS One. 2012;7(12):e44591.

The EPHB6 receptor tyrosine kinase is a metastasis suppressor that is frequently silenced by promoter DNA hypermethylation in non-small cell lung cancer

PURPOSE: Loss of EPHB6 receptor tyrosine kinase expression in early-stage non-small cell lung carcinoma (NSCLC) is associated with the subsequent development of distant metastasis. Here, we analyzed the regulation and function of EPHB6 in lung cancer metastasis.
EXPERIMENTAL DESIGN: The expression levels of EPHB6 were compared among normal lung tissue (n = 9), NSCLC without metastasis (n = 39), and NSCLC with metastasis (n = 39) according to the history of the patients. In addition, EPHB6 expression levels of matched tumor-normal pairs from 24 NSCLC patients were analyzed. The promoter DNA methylation status and its association with the expression levels of EPHB6 were determined among 14 pairs of tumor-normal samples. Metastatic potential of EPHB6 was assessed in vitro and in vivo in a metastasis mouse model. Overexpression and RNA interference (RNAi) approaches were used for analysis of the biological functions of EPHB6.
RESULTS:EPHB6 mRNA and protein levels were significantly reduced in NSCLC tumors compared with matched normal lung tissue. DecreasedEPHB6 expression levels were associated with an increased risk for metastasis development in NSCLC patients. Loss of expression correlated withEPHB6 hypermethylation. EPHB6 expression was induced by 5-aza-2'-deoxycytidine treatment in an NSCLC cell line. Restoration of EPHB6expression in lung adenocarcinoma cells increased adhesion and decreased migration. Reexpression of EPHB6 in lung cancer cells almost entirely abolished metastasis formation in non obese diabetic (NOD)/severe combined immunodeficient mice.
CONCLUSIONS:Taken together, these analyses show that EPHB6 is a metastasis inhibitory gene that is frequently silenced by hypermethylation of its promoter in NSCLC.
Yu J., et al. Clin Cancer Res. 2010 Apr 15;16(8):2275-83.
human soluble EphB6 elisa kit enables to detect human samples from aviscera bioscience
Human SolubleEphrin Type-B Receptor 6 (EphB6)ELISA Kit
Code No.: SK00491-01
Size: 96T
Price: $420.00 USD
Standard Range: 9.4- 600 pg/mL
Sensitivity:5 pg/mL
Sample Type: serum, EDTA Plasma
Sample volume: 100 uL
Dilution factor: Optimal dilutions should be determined by each laboratory for each application
IntraCV: 4-6%
InterCV: 8-12%
Protocol: PDF


Code No.
Price ($)
Soluble Ephrin Type-B Receptor 6 (EphB6) (Human) ELISA Kit SK00491-01 96 T 420.00
Human EphB6, recombinant
10 ug