|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
This review focuses on the function of EphA1, EphA2, and ephrin-A1 in tumors and an establishment of pre-metastatic microenvironment in the lungs.
|
30657619 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Ephrin-A1 overexpression could partially reverse LEF-induced suppression of angiogenesis and subsequent tumor growth inhibition.
|
29367676 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Through the C-X-C chemokine ligand 12 (CXCL12)/CXCR4 signaling pathway, ephrin A1 activation enhances the migration of endothelial progenitor cells to HCC to enable the neovascularization of tumors.
|
28789425 |
2017 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We found that Ephrin B3 was concomitantly expressed with EphA2 and Ephrin A1 with higher Ephrin B3 levels found in non-squamous than in squamous tumors, whereas EphA2 was higher expressed in well-differentiated than in low-differentiated tumors.
|
27533087 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Pharmacologic inhibition of glutaminase activity reduced tumor growth in both ephrin-A1-depleted and EPHA2-overexpressing tumor allografts in vivo Mechanistically, we show that the enhanced proliferation and glutaminolysis in the absence of ephrin-A1 were attributed to increased RhoA-dependent glutaminase activity.
|
26833123 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Patients with EPHA1/EPHA2-positive tumors or with tumors with positive EPHA1 and low EFNA1 immunoreactivity had the shortest survival rates compared to the respective other combinations.
|
25025847 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Released soluble ephrin-A1 in the serum deteriorated the EphA1/ephrin-A1-mediated cell adhesion in the lungs in an endocrine manner, causing lung hyperpermeability that facilitated tumor cell entry into the lungs.
|
23686306 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
These results revealed a possible novel mechanism whereby ephrin-A1 is regulated in tumor microenvironment and promotes angiogenesis through a coordinated cross-talk with PI3K/Akt-dependent eNOS activation which may relate to normal vascular development and tumor neovascularization.
|
24040255 |
2013 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In a previously published report we characterized the expression of the metastasis-associated proteins S100A4, osteopontin (OPN) and ephrin-A1 in a prospectively collected panel of non-small cell lung cancer (NSCLC) tumors.
|
24215488 |
2013 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The effectiveness of targeted delivery of let-7a miR encapsulated ephrin-A1 conjugated LNP (miR-ephrin-A1-LNP) was determined on MPM and NSCLC tumor growth in vitro. miR-ephrin-A1-LNP significantly increased the delivery of let-7a miR in lung cancer cells when compared with free let-7a miR.
|
24293999 |
2013 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We retrospectively evaluated the expression levels of EphA2 and ephrin-A1 in surgically treated pathological (p-) stage I NSCLC tumor samples, and their relation to clinicopathologic features or postoperative prognoses.
|
22236865 |
2012 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We conclude that receptor EphA2 activation by ephrin-A1 induces tumor suppressor gene cdx-2 expression which attenuates cell proliferation, tumor growth and thus may be a promising therapeutic target against NSCLC.
|
22824143 |
2012 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We also show that mouse embryos lacking both Hic1 alleles manifest developmental defects spatially associated with the misexpression of ephrin-A1, and that overexpression of ephrin-A1 is a feature of tumors arising in Hic1 heterozygous mice in which the remaining wild-type allele is epigenetically silenced.
|
20154726 |
2010 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The over-expression of the ephrin-A1 ligand receptor EphA2 is associated with the growth and metastatic potential of tumors.
|
17041885 |
2006 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Immunohistochemical analysis of CD52, AMFR, and Ephrin A1 receptor revealed expression profiles concordant with the microarray data, also with regard to differences between primary tumors and relapses.
|
16325507 |
2005 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
11 (9.3%), 67 (56.8%), 26 (22.0%), and 14 (11.9%) tumors demonstrated negative, weak, moderate, and strong EphA2 protein expressions, respectively, while 3 (2.5%), 67 (56.8%), 32 (27.1%), and 16 (13.8%) tumors were negative, weak, moderate, and strong for Ephrin A-1 protein expression, respectively.
|
16061279 |
2005 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
These findings suggest that the poor prognosis of patients with AFP producing HCC is partially caused by ephrin-A1 expression, which induces expression of genes related to tumour cell growth, angiogenesis, invasion, and metastasis.
|
15888795 |
2005 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The ephrin-A1 ligand and its receptor, EphA2, are expressed during tumor neovascularization.
|
11146556 |
2000 |