@Article{096504016X14813867762123,
AUTHOR = {Yufeng Liu, Zhengliang Cheng, Feng Pan, Weigang Yan},
TITLE = {MicroRNA-373 Promotes Growth and Cellular Invasion in Osteosarcoma  Cells by Activation of the PI3K/AKT–Rac1–JNK Pathway:  The Potential Role in Spinal Osteosarcoma},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {6},
PAGES = {989--999},
URL = {http://www.techscience.com/or/v25n6/56881},
ISSN = {1555-3906},
ABSTRACT = {Spinal osteosarcoma (OS) has been proven to be more difficult to treat owing to potently malignant metastasis. 
The present study aimed to explore the functional role of microRNA (miR)-373 in cell growth and invasion 
of OS cells, as well as its underlying mechanism. The expression of miR-373 was analyzed in spinal OS tissues and cell lines. MG-63 cells were transfected with the miR-373 mimic or inhibitor and/or treated with the 
phosphoinositide 3-kinase (PI3K) (LY294002) inhibitor or Ras-related C3 botulinum toxin substrate 1 (Rac) 
guanosine triphosphate (GTPase) (NSC23766) inhibitor, and then the impact of miR-373 aberrant expression 
on cell growth and invasion was measured, along with the impact of overexpressing miR-373 on the expression 
of p53 and PI3K/AKT pathway-related proteins. We found that miR-373 was specifically upregulated in spinal 
OS tissues (<i>p</i><0.01) and OS cell lines (<i>p</i><0.01 or <i>p</i><0.001). Moreover, miR-373 expression was significantly 
associated with TNM stage (<i>p</i> = 0.035) and tumor size ( <i>p</i> = 0.002). Overexpression of miR-373 promoted 
MG-63 cell viability, migration, invasion, and colony formation (all <i>p</i><0.05), while silencing of miR-373 and 
LY294002 exerted the opposite effects. Additionally, miR-373 overexpression downregulated p53 as well as its 
downstream targeted genes and orderly activated the PI3K/AKT–Rac1–JNK signaling pathway. In conclusion, 
miR-373 promotes growth and cellular invasion in OS cells by activating the PI3K/AKT–Rac1–JNK pathway. 
Therefore, miR-373 might be a candidate for molecular targeted therapy of spinal OS.},
DOI = {10.3727/096504016X14813867762123}
}