Aminoacyl-tRNA synthetases [ARS]-interacting multifunctional protein 2 (AIMP2) 
has been implicated in the control of cell fate and lung cell differentiation. A 
variant of AIMP2 lacking exon 2 (AIMP2-DX2) is expressed in different cancer 
cells. We previously studied the expression level of AIMP2-DX2 in several lung 
cell lines and reported elevated expression levels of AIMP2-DX2 in NCI-H460 and 
NCI-H520. Here, we report that the suppression of AIMP2-DX2 by lentivirus 
mediated short hairpin (sh)RNA (sh-DX2) decreased the rate of glucose uptake and 
glucose transporters (Gluts) in NCI-H460 cells. Down-regulation of AIMP2-DX2 
reduced glycosyltransferase (GnT)-V in the Golgi apparatus, while inducing the 
GnT-V antagonist GnT-III. Down-regulation of AIMP2-DX2 also suppressed the 
epidermal growth factor receptor/mitogen activated protein kinase (EGFR/MAPK) 
signaling pathway, leading to the decrease of the proliferation marker Ki-67 
expression in nuclei. Furthermore, dual luciferase activity reduced capdependent 
protein translation in cells infected with sh-DX2. These results suggest that 
AIMP2-DX2 may be a relevant therapeutic target for lung cancer, and that the 
sh-DX2 lentiviral system can be an appropriate method for lung cancer therapy.