Introduction:
It has been unclear whether STARD13-AS has effects in glioma. The aim of our research was to investigate the effects of STARD13-AS in glioma development and the mechanisms underlying these effects.

Material and methods:
Adjacent normal and tumor tissues were collected for long non-coding RNA (lncRNA) microarray screening. STARD13-AS expression was measured by in situ hybridization (ISH) and reverse-transcription quantitative PCR (RT-qPCR) assays, and correlations between STARD13-AS and clinicopathological parameters and prognosis were analyzed. STARD13-AS transfection of glioma cell lines (U251 and U87) was used to evaluate biological activities of cells. Western blotting (WB) and RT-qPCR assays were used to investigate the underlying mechanisms.

Results:
According to lncRNA microarray screening, ISH, and RT-qPCR, lncRNA STARD13-AS was significantly downregulated in tumor tissues. Low STARD13-AS expression was strongly correlated with poor prognosis and malignant clinicopathology. After STARD13-AS transfection, biological activities of glioma cells were significantly decreased (p < 0.001 for both cell types). WB and RT-qPCR assays showed that protein and mRNA expression levels of cyclin D, cyclin E, N-cadherin, E-cadherin, and vimentin were significantly related to STARD13-AS overexpression (p < 0.001 in all cases).

Conclusions:
STARD13-AS overexpression suppresses the biological activities of glioma cells, indicating that STARD13-AS is a potential target for glioma treatment.