The diagnostic, predictive, and prognostic role of serum epithelial cell adhesion molecule (EpCAM) and vascular cell adhesion molecule-1 (VCAM-1) levels in breast cancer

Tumor Biology ◽  
2014 ◽  
Vol 35 (9) ◽  
pp. 8849-8860 ◽  
Author(s):  
S. Karabulut ◽  
F. Tas ◽  
D. Tastekin ◽  
M. Karabulut ◽  
C. T. Yasasever ◽  
...  
2017 ◽  
Vol 40 (3) ◽  
pp. 199-208 ◽  
Author(s):  
Rohit Sharma ◽  
Rohini Sharma ◽  
Tejinder Pal Khaket ◽  
Chanchala Dutta ◽  
Bornisha Chakraborty ◽  
...  

2012 ◽  
Vol 38 (6) ◽  
pp. 774-779 ◽  
Author(s):  
Mei-Chi Chang ◽  
Li-Deh Lin ◽  
Jenny Zwei-Ching Chang ◽  
Chiung-Fang Huang ◽  
Fu-Hsiung Chuang ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Weiling Leng ◽  
Xiaotian Lei ◽  
Hao Meng ◽  
Xinshou Ouyang ◽  
Ziwen Liang

Our research group firstly discovered endothelial-overexpressed lipopolysaccharide-associated factor 1 (EOLA1, GenBank number AY074889) as a lipopolysaccharide (LPS) responsive gene in ECV304 cells. The previous studies have further demonstrated the association of EOLA1 with metallothionein 2A (MT2A), while the role of EOLA1 during LPS-induced inflammatory response in ECV304 cells is unknown. In this report, we determined the subcellular localization of EOLA1 and the regulatory capacity of EOLA1 on vascular cell adhesion molecule-1 (VCAM-1) in response to LPS in ECV304 cells. Our results show that EOLA1 is broadly diffuse in the cells, and EOLA1 expression is dramatically induced by LPS. EOLA1 knockdown results in significant enhancement of LPS-induced VCAM-1 production. Consistent with this, overexpression of EOLA1 leads to the reduction of LPS-induced VCAM-1 production. Furthermore, MT2A knockdown reduces LPS-induced VCAM-1 production. Collectively, our results demonstrate a negative regulatory role of EOLA1 on LPS-induced VCAM-1 expression involving its association with MT2A in ECV304 cells.


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