Karyopherins mediate the macromolecular transport between the cytoplasm and the 
nucleus and participate in cancer progression. However, the role and mechanism 
of importin-11 (IPO11), a member of the karyopherin family, in glioma 
progression remain undefined. Effects of IPO11 on glioma progression were 
detected using CCK-8, colony formation assay, flow cytometry analysis, caspase-3 
activity assay, and Transwell invasion assay. Western blot analysis was used to 
detect the expression of active caspase-3, active caspase-7, active caspase-9, 
N-cadherin, Vimentin, E-cadherin, β-catenin, and c-Myc. The activity of 
Wnt/β-catenin pathway was evaluated by the T-cell factor/lymphoid enhancer 
factor (TCF/LEF) transcription factor reporter assay. Results showed that IPO11 
knockdown inhibited proliferation and reduced colony number in glioma cells. 
IPO11 silencing promoted the apoptotic rate, increased expression levels of 
active caspase-3, caspase-7, and caspase-9, and enhanced caspase-3 activity. 
Moreover, IPO11 silencing inhibited glioma cell invasion by suppressing 
epithelial-to-mesenchymal transition (EMT). Mechanistically, IPO11 knockdown 
inactivated the Wnt/β-catenin pathway. β-Catenin overexpression abolished the 
effects of IPO11 silencing on the proliferation, apoptosis, and invasion in 
glioma cells. Furthermore, IPO11 silencing blocked the malignant phenotypes and 
repressed the Wnt/β-catenin pathway in vivo. In conclusion, IPO11 knockdown 
suppressed the malignant phenotypes of glioma cells by inactivating the 
Wnt/β-catenin pathway.