Objective The aim of this study was to investigate the expression of PTV1 lnc RNA in gliomas and the mechanism of its interaction with mi R-203 a.Methods U87 and U251 cells were cultured stably and transfected with sh-PTV1 or ov-PTV1, respectively. The proliferative activity of U87 and U251 cells was detected and the transplanted tumor model nude mice were divided into U87 and U251 groups. U87-sh and u251-ov cells were injected into the armpit, then mi R-203 a mic and mi R-203 a inhibitors were administered to detect the changes in the expression of tumorrelated proteins. Results The relative expression of PTV1 in gliomas was significantly higher than that in normal brain tissues, while in GBM it was significantly higher than that in low-grade gliomas. Knockdown of PTV1 significantly inhibited the proliferation of U87 cells, resulting in fewer cell clones; overexpression of r PTV1 significantly promoted the proliferation of U251 cells, resulting in more cell colonies. The dual Luciferase Reporter assay showed that SP2 was a potential target of mi R-203 a. When U87 cells were treated with a mi R-203 a mimic, the expression of SP2 decreased; and when U251 cells were treated with a mi R-203 a inhibitor, the expression of SP2 increased significantly. SP2 was overexpressed in u87-sh cells and the proliferation, migration, and invasion of u87-sh cells were significantly enhanced. U251-ov cells showed the opposite trend. Compared with the control group mice, the tumor volume in u87-sh group mice was significantly smaller and the positive rate of SP2 in tumor tissue was significantly lower. After administration of the mi R-203 a inhibitor, the tumor volume increased gradually and the positive rate of SP2 increased significantly, while u251-ov mice showed the opposite trend. Conclusion lnc RNA PTV1 can be used as a molecule to interfere with mi R-203 a expression in order to downregulate SP2 and to promote the proliferation and invasion of glioma cells. lnc RNA PTV1 may be a
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