@Article{096504016X14732772150343,
AUTHOR = {Hongsheng Dang, Wuzhou Wu, Bo Wang, Cao Cui, Juwei Niu, Jie Chen, Ziqiu Chen, Yi Liu},
TITLE = {CXCL5 Plays a Promoting Role in Osteosarcoma Cell Migration  and Invasion in Autocrine- and Paracrine-Dependent Manners},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {2},
PAGES = {177--186},
URL = {http://www.techscience.com/or/v25n2/56796},
ISSN = {1555-3906},
ABSTRACT = {CXCL5, a CXC-type chemokine, is an important attractant for granulocytic immune cells by binding to its 
receptor CXCR2. Recently, CXCL5/CXCR2 has been found to play an oncogenic role in many human cancers. 
However, the exact role of CXCL5 in osteosarcoma cell migration and invasion has not been revealed. Here we 
found that the protein expression of CXCL5 was significantly increased in osteosarcoma tissues compared with 
that in matched adjacent nontumor tissues. Moreover, the expression of CXCL5 was significantly associated 
with advanced clinical stage and metastasis. Further investigation showed that the CXCL5 expression levels 
were also significantly increased in osteosarcoma cell lines, including Saos-2, MG63, U2OS, and SW1353, 
when compared with those in normal osteoblast hFoB1.19 cells. U2OS cells were further transfected with 
CXCL5-specific siRNA or overexpression plasmid. Knockdown of CXCL5 significantly suppressed U2OS 
cell migration and invasion. On the contrary, overexpression of CXLC5 remarkably promoted the migration 
and invasion of U2OS cells. Interestingly, both exogenous CXCL5 treatment and the conditioned medium of 
CXCL5-overexpressing hFoB1.19 cells could also enhance the migration and invasion of U2OS cells, suggesting that the promoting role of CXCL5 in U2OS cell migration and invasion is also in a paracrine-dependent 
manner. According to these data, our study demonstrates that CXCL5 is upregulated in osteosarcoma and may 
play an oncogenic role in osteosarcoma metastasis. Therefore, CXCL5 may become a potential therapeutic 
target for osteosarcoma treatment.},
DOI = {10.3727/096504016X14732772150343}
}