Mitochondrial
serine hydroxyl-
methyltransferase 2 (SHMT2), participating in the synthesis of mitochondrial
thymidine monophosphate, has been reported to drive
glioma cell survival in
ischemia. However, its clinical relevance in
gliomas remains unclear. In the current study, immunohistochemistry was performed to examine subcellular localization and expression levels of SHMT2
protein in
glioma and non-neoplastic brain tissue specimens. Then, the associations of SHMT2 expression with various clinicopathological features and patients' prognosis were statistically evaluated. The roles of SHMT2 in the proliferation and invasion of
glioma cells after siRNA-SHMT2 vector transfection were also detected by cell counting kit-8 and transwell assays, respectively. Results showed that SHMT2 immunostaining was predominantly localized in the cellular cytoplasm of
tumor cells in
glioma tissues but weakly in non-neoplastic brain tissues. Statistically, SHMT2
protein expression was significantly higher in
glioma tissues than in non-neoplastic brain tissues (P<0.001). In addition, SHMT2 overexpression more frequently occurred in
glioma patients with an advanced grade of
malignancy (P<0.001) and poor prognosis (P=0.001). Notably, multivariate analysis based on a Cox regression model identified SHMT2 expression as an independent prognostic factor for
glioma patients (P=0.01). Functionally, SHMT2 knockdown efficiently suppressed the proliferation (P=0.02) and invasion (P<0.001) of
glioma cells in vitro. In conclusion, our findings suggest that SHMT2 may function as an oncogene in
glioma development and progression. Clinically, SHMT2 may serve as a prognostic factor and as a potential therapeutic target for human
gliomas.