@Article{096504018X15172227703244,
AUTHOR = {Haoran Wu, Xugang Wang, Naixin Mo, Liang Zhang, Xiaoliang Yuan, Zhong Lü},
TITLE = {B7-Homolog 4 Promotes Epithelial–Mesenchymal Transition and Invasion of  Bladder Cancer Cells via Activation of Nuclear Factor-κB},
JOURNAL = {Oncology Research},
VOLUME = {26},
YEAR = {2018},
NUMBER = {8},
PAGES = {1267--1274},
URL = {http://www.techscience.com/or/v26n8/56756},
ISSN = {1555-3906},
ABSTRACT = {B7-homolog 4 (B7-H4), a member of the B7 family of costimulatory molecules, has been reported to be 
upregulated in urothelial cell carcinoma. This study was conducted to explore the biological role of B7-H4 
in the aggressiveness of bladder cancer and the associated molecular mechanism. We found that the mRNA 
and protein levels of B7-H4 were significantly greater in bladder cancer cell lines than in SV-HUC-1 (normal 
human urothelial cells). Overexpression of B7-H4 significantly promoted bladder cancer cell migration and 
invasion, whereas knockdown of B7-H4 exerted an opposite effect. However, the growth of bladder cancer 
cells was not altered by B7-H4 overexpression or knockdown. Overexpression of B7-H4 promoted epithelial–
mesenchymal transition (EMT), as evidenced by decreased E-cadherin and increased vimentin expression. The EMT inducers Twist1 and Snail were upregulated by B7-H4 overexpression and downregulated 
by B7-H4 silencing. Mechanistically, overexpression of B7-H4 induced the activation of NF-kB signaling. 
Pharmacological inhibition of NF-kB partially prevented B7-H4-mediated bladder cancer cell invasion. Taken 
together, B7-H4/NF-kB signaling is involved in the EMT and invasion of bladder cancer cells and represents a 
new candidate target for the treatment of bladder cancer.},
DOI = {10.3727/096504018X15172227703244}
}