BACKGROUND: Determining the expression levels of neuroglial antigen 2 (NG2) in 
glioma cell lines and to evaluate the potential contribution of NG2 to 
cilengitide response were aimed.
MATERIALS AND METHODS: Endogenous expression level of NG2 was determined using 
quantitative reverse transcription polymerase chain reaction and immunoblotting. 
Cilengitide responses of the cells were monitored to determine half maximal 
inhibitory concentration values. Whether the suppression of NG2 expression 
alters the response of A172 cells to cilengitide was examined.
RESULTS: The effect of cilengitide on inducing apoptosis of the cells was 
determined by TUNEL staining. High mRNA and protein expression of NG2 was 
detected in A172 and U-87MG cells, while T98G, M059K and M059J cells 
demonstrated low levels of NG2. A172, U-87MG and positive control MG-63 were 
relatively sensitive to cilengitide compared to T98G, M059K and M059J. MG-63, 
A172 and U-87MG were unexpectedly found to be more susceptible to cilengitide. 
In addition, NG2 knock-down showed no significant difference in cell death 
between small interfering RNA (siRNA)-transfected and cilengitide-treated 
groups. The results showed that cilengitide caused detachment and subsequently 
initiated apoptosis. Glioma cell lines express variable levels of NG2 and differ 
in their responses to cilengitide. Although increased numbers of apoptotic cells 
were found in untransfected cells compared to siRNA-transfected cells upon 
exposed to cilengitide, the difference was not documented to be significant 
between two groups.
CONCLUSION: It may be proposed that the combination therapy of NG2 suppression 
and cilengitide treatment showed no considerable effect on glioblastoma compared 
to cilengitide therapy alone. Response to therapy may be further improved by 
targeting other factors act in concert in this signaling pathway.