--- - |2- We found that inhibition of nuclear paraspeckle assembly transcript 1 (NEAT1) repressed glioma development via sponging miR‐107. The correlation between NEAT1 and miR‐107 was validated in our study, and cyclin dependent kinase 14 (CDK14) was targeted by miR‐107 by using bioinformatics analysis. All these data revealed that NEAT1/miR‐107/CDK14 axis was involved in glioma development Abstract Aberrant expressions of long noncoding RNAs (lncRNAs) contribute to carcinogenesis via regulating tumor suppressors or oncogenes. LncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) has been recognized as an oncogene to promote tumor progression of many cancers. However, the function of NEAT1 in glioma remains poorly discovered. Currently, we focused on the role of NEAT1 in glioma. Here, we found that NEAT1 was greatly upregulated in glioma cells compared with normal human astrocytes (NHAs). Meanwhile, miR‐107 was significantly downregulated in glioma cell lines. Then, we observed that knockdown of NEAT1 suppressed the growth and invasion of glioma cells including U251 and SW1783 cells. Reversely, overexpression of NEAT1 dramatically induced glioma cell survival, increased cell colony formation, and promoted cell invasion ability. Subsequently, bioinformatics analysis was performed to predict the correlation between NEAT1 and miR‐107. Moreover, it was revealed that NEAT1 could modulate miR‐107 via serving as an endogenous sponge of miR‐107. The direct binding correlation between NEAT1 and miR‐107 was validated in our study. In addition, cyclin dependent kinase 14 (CDK14) was predicted as an messenger RNA target of miR‐107 and the association between them was confirmed in our research. Moreover, we implied that NEAT1 demonstrated its biological functions via regulating miR‐107 and CDK14 in vivo. In summary, our findings indicated that NEAT1/miR‐107/CDK14 axis participated in glioma development. NEAT1 could act as a significant prognostic biomarker in glioma progression. - 'Journal of Cellular Physiology, EarlyView. '