Evidence has revealed that long non-coding RNAs (lncRNAs) are involved in
carcinogenesis and
tumor progression. lncRNAs play an important role in regulation of numerous cellular processes including cell proliferation, apoptosis, cell cycle, differentiation, and motility. Several studies have demonstrated that
lncRNA EPIC1 governs cell growth, cell cycle, migration, invasion, and drug resistance in human
malignancies. However, the role of EPIC1 and its underlying molecular mechanisms in
glioma have not been investigated. In this study, we determined the function of EPIC1 in
glioma cells via upregulation or downregulation of EPIC1. We further dissected the mechanism of EPIC1-mediated
tumor progression in
glioma. Our results showed that inhibition of EPIC1 suppressed cell viability, induced apoptosis, inhibited cell invasion, and increased cell sensitivity to
temozolomide in
glioma cells. Consistently, overexpression of EPIC1 exhibited the opposite effects in
glioma cells. Moreover, our data suggest that EPIC1 exerts its
biological functions via targeting Cdc20 in
glioma cells. In line with this, overexpression of Cdc20 reversed the EPIC1-mediated
tumor progression in
glioma cells. Therefore, targeting EPIC1 might be a useful approach for
glioma treatment.