Abstract
Long noncoding RNA (lncRNA) DUXAP10 has been shown to act as an oncogene in various tumors; however, its roles in glioma progression have never been established. Here, we show that DUXAP10 is overexpressed in glioma tissues and cells. Loss of function experiments reveal that DUXAP10 knockdown has little effects on glioma cell viability, but significantly reduces the stemness of glioma cells, which is characterized as the decrease of stemness marker expression, tumor sphere-forming ability, and ALDH activity. RNA immunoprecipitation and immunofluorescence assays indicate that DUXAP10 can directly interact with HuR protein and suppress the cytoplasm-nuclear translocation of HuR, which subsequently enhances Sox12 mRNA stability in cytoplasm and thus increases Sox12 expression. Further rescuing experiments show that the HuR/Sox12 axis is responsible for DUXAP10-mediated effects on glioma cell stemness.