Objective The aim of this study was to investigate the expression of PTV1 lncRNA in gliomas and themechanism of its interaction with miR-203a.Methods U87 and U251 cells were cultured stably and transfected with sh-PTV...Objective The aim of this study was to investigate the expression of PTV1 lncRNA in gliomas and themechanism of its interaction with miR-203a.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 micewere divided into U87 and U251 groups. U87-sh and u251-ov cells were injected into the armpit, thenmiR-203a mic and miR-203a inhibitors were administered to detect the changes in the expression of tumorrelatedproteins.Results The relative expression of PTV1 in gliomas was significantly higher than that in normal braintissues, while in GBM it was significantly higher than that in low-grade gliomas. Knockdown of PTV1significantly inhibited the proliferation of U87 cells, resulting in fewer cell clones;overexpression of rPTV1significantly promoted the proliferation of U251 cells, resulting in more cell colonies. The dual LuciferaseReporter assay showed that SP2 was a potential target of miR-203a. When U87 cells were treated with amiR-203a mimic, the expression of SP2 decreased;and when U251 cells were treated with a miR-203ainhibitor, the expression of SP2 increased significantly. SP2 was overexpressed in u87-sh cells and theproliferation, migration, and invasion of u87-sh cells were significantly enhanced. U251-ov cells showedthe opposite trend. Compared with the control group mice, the tumor volume in u87-sh group mice wassignificantly smaller and the positive rate of SP2 in tumor tissue was significantly lower. After administrationof the miR-203a inhibitor, the tumor volume increased gradually and the positive rate of SP2 increasedsignificantly, while u251-ov mice showed the opposite trend.Conclusion lncRNA PTV1 can be used as a molecule to interfere with miR-203a expression in order todownregulate SP2 and to promote the proliferation and invasion of glioma cells. lncRNA PTV1 may be anew biomarker and therapeutic target for glioma.展开更多
基金Supported by a grant from the general program of NSFC(No.81472965)。
文摘Objective The aim of this study was to investigate the expression of PTV1 lncRNA in gliomas and themechanism of its interaction with miR-203a.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 micewere divided into U87 and U251 groups. U87-sh and u251-ov cells were injected into the armpit, thenmiR-203a mic and miR-203a inhibitors were administered to detect the changes in the expression of tumorrelatedproteins.Results The relative expression of PTV1 in gliomas was significantly higher than that in normal braintissues, while in GBM it was significantly higher than that in low-grade gliomas. Knockdown of PTV1significantly inhibited the proliferation of U87 cells, resulting in fewer cell clones;overexpression of rPTV1significantly promoted the proliferation of U251 cells, resulting in more cell colonies. The dual LuciferaseReporter assay showed that SP2 was a potential target of miR-203a. When U87 cells were treated with amiR-203a mimic, the expression of SP2 decreased;and when U251 cells were treated with a miR-203ainhibitor, the expression of SP2 increased significantly. SP2 was overexpressed in u87-sh cells and theproliferation, migration, and invasion of u87-sh cells were significantly enhanced. U251-ov cells showedthe opposite trend. Compared with the control group mice, the tumor volume in u87-sh group mice wassignificantly smaller and the positive rate of SP2 in tumor tissue was significantly lower. After administrationof the miR-203a inhibitor, the tumor volume increased gradually and the positive rate of SP2 increasedsignificantly, while u251-ov mice showed the opposite trend.Conclusion lncRNA PTV1 can be used as a molecule to interfere with miR-203a expression in order todownregulate SP2 and to promote the proliferation and invasion of glioma cells. lncRNA PTV1 may be anew biomarker and therapeutic target for glioma.
