Our previous work has shown that S100A9 promotes the growth of
glioma cells. The aim of this study was to investigate S100A9 expression in
glioma cells and to explore the potential of
NSAIDs in the inhibition of S100A9. The levels of S100A9 were analyzed in five normal human brain tissues and 109
astrocytomas by immunohistochemical analysis. In addition, S100A9 levels were detected in normal human astrocytes,
glioma cell lines, and six pairs of matched
astrocytoma tissues by reverse transcription-PCR or western blotting analysis.
After treatment with 4, 8, and 16 mmol/l
aspirin, cell viability, early apoptosis rate, and S100A9 levels were quantified. Cell viability and the changes in S100A9 levels were also examined in
glioma cells exposed to a
cyclooxygenase-2 inhibitor,
NS-398, alone and in combination with
prostaglandin E2. We found that S100A9 was upregulated in
astrocytomas and was significantly (P<0.05) correlated with histologic grades.
S100A9 protein levels were also elevated in six
astrocytomas compared with matched adjacent noncancerous tissues. Both S100A9
mRNA and
protein levels were higher in
glioma cell lines than in normal human astrocytes (P<0.05).
Aspirin treatment inhibited cell proliferation and caused early apoptosis in
glioma, coupled with reduced S100A9 levels. Treatment with
NS-398 decreased cell growth and expression of S100A9 in
glioma cells; these effects were partially reversed by exogenous
prostaglandin E2. These results suggest overexpression of S100A9 in
glioma cells.
Aspirin may be a novel candidate for targeted prevention of S100A9 overexpression in
glioma cells.