
@Article{096504018X15155538502359,
AUTHOR = {Xuejian Liu, Xia Wu, Yanming Wang, Yuhua Li, Xiangli Chen, Wenchuan Yang, Lihua Jiang},
TITLE = {CD47 Promotes Human Glioblastoma Invasion Through  Activation of the PI3K/Akt Pathway},
JOURNAL = {Oncology Research},
VOLUME = {27},
YEAR = {2019},
NUMBER = {4},
PAGES = {415--422},
URL = {http://www.techscience.com/or/v27n4/48554},
ISSN = {1555-3906},
ABSTRACT = {Cluster of differentiation 47 (CD47) overexpression is common in various malignancies. This study investigated whether CD47 promotes human glioblastoma invasion and, if so, the underlying mechanisms involved. 
CD47 expression was found to be stronger in tissues of patients with glioblastoma and in various cancer cell 
lines than in normal controls. CD47 downregulation via siRNA suppressed invasion in vitro, whereas CD47 
overexpression through plasmid transfection exerted the opposite effect. However, overexpression or knocking 
down of CD47 had no effect on cell proliferation. Moreover, CD47 expression was related to Akt phosphorylation at the cellular molecular level. Suppression of Akt with a specific inhibitor impaired the invasion ability 
of CD47-overexpressing cells, indicating that stimulation of the PI3K/Akt pathway served as the downstream 
regulator of CD47-triggered invasion. These results suggest that CD47 might be a useful predictor of poor 
prognosis and metastasis and a potential target for treating glioblastomas.},
DOI = {10.3727/096504018X15155538502359}
}



