LAUSR

OBJECTIVE The aim of this study was to elucidate whether FOXD2-AS1 stimulated glioma progression by inhibiting the P53 level. PATIENTS AND METHODS FOXD2-AS1 expression in glioma tissues and cell lines was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Meanwhile, FOXD2-AS1 expression in glioma patients with different tumor tissues and tumor staging was examined as well. The subcellular distribution of FOXD2-AS1 was analyzed. RNA Binding Protein Immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) assay were applied to explore the interaction between FOXD2-AS1 and P53. Furthermore, the influences of FOXD2-AS1 and P53 on the viability and colony formation abilities of LN229 and U87 cells were assessed. RESULTS FOXD2-AS1 was significantly upregulated in glioma tissues and cells. The expression level of FOXD2-AS1 was positively correlated with tumor size and staging of glioma. FOXD2-AS1 was mainly distributed in the nucleus, which could attenuate recruitment ability to P53 by bounding to EZH2. The silence of FOXD2-AS1 significantly decreased the viability and colony formation abilities of glioma cells. However, the attenuated proliferative ability was partially reversed by P53 knockdown. CONCLUSIONS FOXD2-AS1 stimulated the proliferation of glioma by inhibiting P53, thus aggravating the progression of glioma.