Open AccessCD47 Promotes Human Glioblastoma Invasion Through Activation of the PI3K/Akt Pathway
Author(s) -
Xuejian Liu,
Xia Wu,
Yanming Wang,
Yuhua Li,
Xiangli Chen,
Wenchuan Yang,
Lihua Jiang
Publication year - 2019
Publication title -
oncology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 57
eISSN - 1555-3906
pISSN - 0965-0407
DOI - 10.3727/096504018x15155538502359
Subject(s) - cd47 , pi3k/akt/mtor pathway , protein kinase b , cancer research , downregulation and upregulation , transfection , biology , phosphorylation , cell culture , regulator , microbiology and biotechnology , signal transduction , cell , gene , genetics
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.